Microbial consortium and uses thereof

Abstract

To provide microbial compositions and methods of using the same.SOLUTION: Microbial compositions provided include, inter alia, therapeutically effective amounts of Lactobacillus johnsonii, Faecalibacterium prausnitzii, Akkermansia muciniphila, Myxococcus xanthus and Pediococcus pentosaceus and are particularly useful for methods of treating and preventing inflammatory diseases.SELECTED DRAWING: None

Description

[Technical Field]

[0001] CROSS-REFERENCE TO RELATED APPLICATIONS This application claims the benefit of priority to U.S. Provisional Patent Application No. 62 / 304,087, filed March 4, 2016, which is incorporated herein by reference in its entirety for all purposes. STATEMENT REGARDING RIGHTS TO INVENTIONS MADE UNDER FEDERALLY SPONSORED RESEARCH AND DEVELOPMENT

[0002] This invention was made with government support under Grant Nos. R21 AT004732, P01 AI089473, and HL080074 awarded by the National Institutes of Health. The government has certain rights in this invention. Incorporation by reference to sequence listing

[0003] The contents of the text file named "48536-575001WO_SequenceListing.TXT", created on March 3, 2017, and having a size of 107,536 bytes, are incorporated herein by reference in their entirety. [Background technology]

[0004] Recent studies have provided evidence that the microbial community present in the human gut plays an important role in the development and regulation of host immune responses. For example, the presence of specific Clostridium species has been shown to induce specific T cell repertoires [Atarashi et al. (2011) Induction of colonic regulatory T cells by indigenous Clostridium species. Science 331(6015):337-341]. Despite the complexity of the gut microbiome, the presence or absence of specific bacterial species can dramatically alter the adaptive immune environment. [Prior art documents] [Non-patent literature]

[0005] [Non-Patent Document 1] Atarashi et al. (2011) Induction of colonic regulatory T cells by indigenous Clostridium species. Science 331(6015):337-341 Summary of the Invention [Means for solving the problem]

[0006] Provided herein are novel methods and microbial compositions comprising Lactobacillus johnsonii, Faecalibacterium prausnitzii, Akkermansia muciniphila, Myxococcus xanthus, and Pediococcus pentosaceus that are surprisingly useful in the treatment of dysbiosis, infection, and inflammatory diseases. Certain aspects provide methods and compositions comprising a bacterial population comprising, consisting essentially of, or consisting of 1, 2, 3, 4, 5, 6, 7, or 8 (or at least 1, 2, 3, 4, 5, 6, 7, or 8) bacterial species. In embodiments, the bacterial population comprises, consists essentially of, or consists of any one, two, three, four, five, six, seven, or eight of Lactobacillus sp., Faecalibacterium sp., Akkermansia sp., Myxococcus sp., Cystobacter sp., Pediococcus sp., Bifidobacterium sp., and Clostridium sp. In embodiments, the bacterial population comprises Lactobacillus sp. and Faecalibacterium prausnitzii. In embodiments, the bacterial population comprises Lactobacillus sp. and Faecalibacterium prausnitzii. In some embodiments, the bacterial population includes Lactobacillus sp. and Myxococcus xanthus. In embodiments, the bacterial population includes Lactobacillus sp. and Cystobacter fuscus. In embodiments, the bacterial population includes Lactobacillus sp. and Pediococcus pentosaceus, Pediococcus acidilactici, Pediococcus damnosus, Pediococcus ethanolidurans, or Pediococcus parvulus. In embodiments, the bacterial population includes Lactobacillus sp. and Bifidobacterium bifidum, Bifidobacterium pseudolongum, Bifidobacterium saeculare, or Bifidobacterium subtile. In embodiments, the bacterial population includes Lactobacillus sp. and Clostridium hiranonis. In embodiments, Lactobacillus sp. is Lactobacillus johnsonii, Lactobacillus rhamnosus, Lactobacillus zeae, Lactobacillus acidipiscis, Lactobacillus acidophilus, Lactobacillus agilis, Lactobacillus aviarius, Lactobacillus brevis, Lactobacillus coleohominis, Lactobacillus crispatus, Lactobacillus crustorum, Lactobacillus curvatus, Lactobacillus diolivorans, Lactobacillus farraginis, Lactobacillus fermentum, Lactobacillus fuchuensis, Lactobacillus harbinensis, Lactobacillus helveticus, Lactobacillus hilgardii, Lactobacillus intestinalis, Lactobacillus jensenii, Lactobacillus kefiranofaciens, Lactobacillus kefiri, Lactobacillus lindneri, Lactobacillus mali, Lactobacillus manihotivorans, Lactobacillus mucosae, Lactobacillus oeni, Lactobacillus oligofermentans, Lactobacillus panis, Lactobacillus pantheris, Lactobacillus parabrevis, Lactobacillus paracollinoides, Lactobacillus parakefiri, Lactobacillus paraplantarum, Lactobacillus pentosus, Lactobacillus pontis, Lactobacillus reuteri, Lactobacillus rossiae, Lactobacillus salivarius, Lactobacillus siliginis, Lactobacillus sucicola, Lactobacillus vaccinostercus, Lactobacillus vaginalis, Lactobacillus vini, Lactococcus garvieae or Lactobacillus lactis. In multiple embodiments, Lactobacillus sp. agilis, Lactobacillus aviarius, Lactobacillus brevis, Lactobacillus coleohominis, Lactobacillus crispatus, Lactobacillus crustorum, Lactobacillus curvatus, Lactobacillus diolivorans, Lactobacillus farraginis, Lactobacillus fermentum, Lactobacillus fuchuensis, Lactobacillus harbinensis, Lactobacillus helveticus, Lactobacillus hilgardii, Lactobacillus intestinalis, Lactobacillus jensenii, Lactobacillus kefiranofaciens, Lactobacillus kefiri, Lactobacillus lindneri, Lactobacillus mali, Lactobacillus manihotivorans, Lactobacillus mucosae, Lactobacillus oeni, Lactobacillus oligofermentans, Lactobacillus panis, Lactobacillus pantheris, Lactobacillus parabrevis, Lactobacillus paracollinoides, Lactobacillus parakefiri, Lactobacillus paraplantarum, Lactobacillus pentosus, Lactobacillus pontis, Lactobacillus reuteri, Lactobacillus rossiae, Lactobacillus salivarius, Lactobacillus siliginis, Lactobacillus sucicola, Lactobacillus vaccinostercus, Lactobacillus vaginalis, Lactobacillus vini, Lactococcus garvieae, Lactococcus lactis, Faecalibacterium prausnitzii, Akkermansia muciniphila, Myxococcus xanthus, Cystobacter fuscus, Pediococcus pentosaceus, Pediococcus acidilactici, Pediococcus damnosus, Pediococcus ethanolidurans and Pediococcus In some embodiments, the bacterial population comprises at least 1, 2, 3, 4, 5, 6, 7, 8, 9, or 10, or 1-5, 1-10, 1-5, or 1-20 of any combination of Lactobacillus johnsonii, Faecalibacterium prausnitzii, Akkermansia muciniphila, Myxococcus xanthus, and / or Pediococcus pentosaceus.

[0007] In some aspects, methods are provided for administering isolated bacteria. In embodiments, the methods include administering isolated bacteria such as Lactobacillus sp., Faecalibacterium In some embodiments, the method comprises administering to the subject an effective amount of a bacterial population comprising Lactobacillus sp., Faecalibacterium sp., Akkermansia sp., Myxococcus sp., and / or Pediococcus sp. In some embodiments, the method comprises administering to the subject an effective amount of a bacterial population comprising Lactobacillus sp., Faecalibacterium sp., Akkermansia sp., Cystobacter sp., and / or Pediococcus sp. In some embodiments, the bacterial population comprises Lactobacillus johnsonii, Faecalibacterium prausnitzii, Akkermansia muciniphila, Myxococcus xanthus and / or Pediococcus pentosaceus. In embodiments, the bacterial population further comprises Bifidobacterium sp. or Clostridium sp. In embodiments, the bacterial population further comprises Bifidobacterium sp. or Clostridium hiranonis.

[0008] In some aspects, methods of bacterial supplementation are provided. In some embodiments, the methods include administering to a subject an effective amount of a bacterial population comprising Lactobacillus sp., Faecalibacterium sp., Akkermansia sp., Myxococcus sp., and / or Pediococcus sp. In some embodiments, the methods include administering to a subject an effective amount of a bacterial population comprising Lactobacillus sp., Faecalibacterium sp., Akkermansia sp., Cystobacter sp., and / or Pediococcus sp. In some embodiments, the bacterial population comprises Lactobacillus johnsonii, Faecalibacterium prausnitzii, Akkermansia muciniphila, Myxococcus xanthus, and / or Pediococcus pentosaceus. In some embodiments, the bacterial population further comprises Bifidobacterium sp. or Clostridium sp. In embodiments, the bacterial population further comprises Bifidobacterium sp. or Clostridium hiranonis.

[0009] In some aspects, methods of treating or preventing inflammation in a subject in need thereof are provided. In some embodiments, the methods comprise administering to the subject an effective amount of a bacterial population comprising Lactobacillus sp., Faecalibacterium sp., Akkermansia sp., Myxococcus sp., and / or Pediococcus sp. In some embodiments, the methods comprise administering to the subject an effective amount of a bacterial population comprising Lactobacillus sp., Faecalibacterium sp., Akkermansia sp., Myxococcus sp., and / or Pediococcus sp. The method includes administering to the subject an effective amount of a bacterial population comprising Lactobacillus johnsonii, Faecalibacterium prausnitzii, Akkermansia muciniphila, Myxococcus xanthus, and / or Pediococcus pentosaceus. In embodiments, the bacterial population further comprises Bifidobacterium sp. or Clostridium sp. In embodiments, the bacterial population further comprises Bifidobacterium sp. or Clostridium hiranonis.

[0010] In some embodiments, a microbial composition is provided. In some embodiments, the microbial composition comprises Lactobacillus sp., Faecalibacterium sp., Akkermansia sp., Myxococcus sp., and / or Pediococcus sp. In some embodiments, the microbial composition comprises Lactobacillus sp., Faecalibacterium sp., Akkermansia sp., Cystobacter sp., and / or Pediococcus sp. In some embodiments, the composition comprises Lactobacillus johnsonii, Faecalibacterium prausnitzii, Akkermansia muciniphila, Myxococcus xanthus, Pediococcus pentosaceus, and a biological carrier suitable for intestinal administration. In some embodiments, the bacterial population further comprises Bifidobacterium sp. or Clostridium sp. In embodiments, the bacterial population further comprises Bifidobacterium sp. or Clostridium hiranonis.

[0011] In some embodiments, a microbial composition is provided. In some embodiments, the microbial composition comprises a Lactobacillus sp., a Faecalibacterium sp., an Akkermansia sp., a Myxococcus sp., and / or a Pediococcus sp. In some embodiments, the microbial composition comprises a Lactobacillus sp., a Faecalibacterium sp., an Akkermansia sp., a Cystobacter sp., and / or a Pediococcus sp. In some embodiments, the composition comprises a Lactobacillus johnsonii, a Faecalibacterium prausnitzii, an Akkermansia muciniphila, a Myxococcus xanthus, or a Pediococcus pentosaceus and a biological carrier suitable for intestinal administration. In some embodiments, the bacterial population further comprises a Bifidobacterium sp. or a Clostridium sp. In embodiments, the bacterial population further comprises Bifidobacterium sp. or Clostridium hiranonis.

[0012] In some aspects, pharmaceutical compositions are provided. In some embodiments, the pharmaceutical compositions comprise Lactobacillus sp., Faecalibacterium sp., Akkermansia sp., Myxococcus sp., and / or Pediococcus sp. In some embodiments, the pharmaceutical compositions comprise Lactobacillus sp., Faecalibacterium sp., Akkermansia sp., Cystobacter sp., and / or Pediococcus sp. In some embodiments, pharmaceutical compositions are provided comprising a therapeutically effective amount of Lactobacillus johnsonii, Faecalibacterium prausnitzii, Akkermansia muciniphila, Myxococcus xanthus, and Pediococcus pentosaceus, and a pharmaceutically acceptable excipient. In some embodiments, the bacterial population further comprises Bifidobacterium sp. or Clostridium sp. In embodiments, the bacterial population further comprises Bifidobacterium sp. or Clostridium hiranonis.

[0013] In some aspects, methods of treating or preventing an inflammatory disease in a subject in need thereof are provided. In some embodiments, the methods comprise administering to the subject an effective amount of a bacterial population comprising Lactobacillus sp., Faecalibacterium sp., Akkermansia sp., Myxococcus sp., and / or Pediococcus sp. In some embodiments, the methods comprise administering to the subject an effective amount of a bacterial population comprising Lactobacillus sp., Faecalibacterium sp., Akkermansia sp., Cystobacter sp., and / or Pediococcus sp. The methods comprise administering to the subject therapeutically effective amounts of Lactobacillus johnsonii, Faecalibacterium prausnitzii, Akkermansia muciniphila, Myxococcus xanthus, and Pediococcus pentosaceus. In embodiments, the bacterial population further comprises a Bifidobacterium sp. or a Clostridium sp. In embodiments, the bacterial population further comprises a Bifidobacterium sp. or a Clostridium hiranonis.

[0014] In some aspects, methods are provided for increasing anti-inflammatory metabolites in a subject in need thereof. In some embodiments, the methods comprise administering to the subject an effective amount of a bacterial population comprising Lactobacillus sp., Faecalibacterium sp., Akkermansia sp., Myxococcus sp., and / or Pediococcus sp. In some embodiments, the methods comprise administering to the subject an effective amount of a bacterial population comprising Lactobacillus sp., Faecalibacterium sp., Akkermansia sp., Cystobacter sp., and / or Pediococcus sp. In some embodiments, the method comprises administering to the subject a therapeutically effective amount of a bacterial population comprising Lactobacillus johnsonii, Faecalibacterium prausnitzii, Akkermansia muciniphila, Myxococcus xanthus, and Pediococcus sp. The method includes administering to the subject Bifidobacterium sp. or Clostridium sp. In several embodiments, the bacterial population further comprises Bifidobacterium sp. or Clostridium hiranonis.

[0015] In some aspects, methods are provided for reducing pro-inflammatory metabolites in a subject in need thereof. In some embodiments, the methods comprise administering to the subject an effective amount of a bacterial population comprising Lactobacillus sp., Faecalibacterium sp., Akkermansia sp., Myxococcus sp., and / or Pediococcus sp. In some embodiments, the methods comprise administering to the subject an effective amount of a bacterial population comprising Lactobacillus sp., Faecalibacterium sp., Akkermansia sp., Cystobacter sp., and / or Pediococcus sp. In some embodiments, the methods comprise administering to the subject a therapeutically effective amount of Lactobacillus johnsonii, Faecalibacterium prausnitzii, Akkermansia muciniphila, Myxococcus xanthus, and Pediococcus pentosaceus. In embodiments, the bacterial population further comprises Bifidobacterium sp. or Clostridium sp. In embodiments, the bacterial population further comprises Bifidobacterium sp. sp. or Clostridium hiranonis.

[0016] In one aspect, a method for detecting an anti-inflammatory metabolite in a subject having or at risk of developing an inflammatory disease is provided, the method comprising (i) obtaining a biological sample from the subject, and (ii) determining the expression level of the anti-inflammatory metabolite in the biological sample.

[0017] In one aspect, a method for detecting a pro-inflammatory metabolite in a subject having or at risk of developing an inflammatory disease is provided, the method comprising (i) obtaining a biological sample from the subject, and (ii) determining the expression level of the pro-inflammatory metabolite in the biological sample.

[0018] In one aspect, a method of determining whether a subject has or is at risk of developing an inflammatory disease is provided, comprising: (i) detecting the expression level of one or more anti-inflammatory or pro-inflammatory metabolites in the subject; (ii) determining whether the expression level is elevated or decreased relative to a standard control, wherein an elevated expression level of a pro-inflammatory metabolite or a decreased expression level of an anti-inflammatory metabolite relative to the standard control indicates that the subject has or is at risk of developing an inflammatory disease; and (iii) determining whether the subject has or is at risk of developing an inflammatory disease based at least in part on the expression levels in step (ii).

[0019] In one aspect, a method of determining whether a subject has or is at risk of developing an inflammatory disease is provided, comprising: (i) detecting an expression level of one or more pro-inflammatory metabolites in the subject; (ii) determining whether the expression level is elevated or decreased relative to a standard control, wherein an elevated expression level of a pro-inflammatory metabolite relative to the standard control indicates that the subject has or is at risk of developing an inflammatory disease; and (iii) determining whether the subject has or is at risk of developing an inflammatory disease based at least in part on the expression level in step (ii).

[0020] In one aspect, a method of determining whether a subject has or is at risk of developing an inflammatory disease is provided, comprising: (i) detecting the expression level of one or more anti-inflammatory metabolites in the subject; (ii) determining whether the expression level is elevated or decreased relative to a standard control, wherein a decreased expression level of the anti-inflammatory metabolite relative to the standard control indicates that the subject has or is at risk of developing an inflammatory disease; and (iii) determining whether the subject has or is at risk of developing an inflammatory disease based at least in part on the expression level in step (ii).

[0021] In one aspect, a method for monitoring the effect of treatment on an inflammatory disease in a subject undergoing treatment or a patient treated for an inflammatory disease is provided, comprising the steps of (i) determining a first expression level of an anti-inflammatory metabolite in the subject at a first time point, (ii) determining a second expression level of the anti-inflammatory metabolite in the subject at a second time point, and (iii) comparing the second expression level of the anti-inflammatory metabolite to the first expression level of the anti-inflammatory metabolite, thereby determining the effect of treatment on the inflammatory disease in the subject.

[0022] In one aspect, a method of monitoring the effect of treatment on an inflammatory disease in a subject undergoing treatment or a patient treated for an inflammatory disease is provided, the method comprising the steps of (i) determining a first expression level of a pro-inflammatory metabolite in the subject at a first time point, (ii) determining a second expression level of the pro-inflammatory metabolite in the subject at a second time point, and (iii) comparing the second expression level of the pro-inflammatory metabolite to the first expression level of the pro-inflammatory metabolite, thereby determining the effect of treatment on the inflammatory disease in the subject.

[0023] In one aspect, a method for determining inflammatory disease activity in a subject is provided, the method comprising: (i) detecting an expression level of one or more anti-inflammatory metabolites in the subject; (ii) determining whether the expression level is modulated compared to a standard control, thereby determining the inflammatory disease activity in the subject; and (iii) determining the inflammatory disease activity in the subject based at least in part on the expression level in step (ii).

[0024] In one aspect, a method for determining inflammatory disease activity in a subject is provided, comprising: (i) detecting an expression level of one or more pro-inflammatory metabolites in the subject; (ii) determining whether the expression level is modulated relative to a standard control, thereby determining inflammatory disease activity in the subject; and (iii) determining inflammatory disease activity in the subject based at least in part on the expression level in step (ii). In an embodiment of the present invention, for example, the following items are provided: (Item 1) A method for treating or preventing dysbiosis in a subject in need thereof, comprising administering to the subject an effective amount of a bacterial population comprising Lactobacillus sp., Faecalibacterium sp., Akkermansia sp., Myxococcus sp., and Pediococcus sp. (Item 2) Item 2. The method according to Item 1, wherein (i) the Lactobacillus sp. is Lactobacillus johnsonii, (ii) the Faecalibacterium sp. is Faecalibacterium prausnitzii, (iii) the Akkermansia sp. is Akkermansia muciniphila, (iv) the Myxococcus sp. is Myxococcus xanthus, and (v) the Pediococcus sp. is Pediococcus pentosaceus. (Item 3) (i) the Lactobacillus sp. is Lactobacillus zeae, Lactobacillus acidipiscis, Lactobacillus acidophilus, Lactobacillus agilis, Lactobacillus aviarius, Lactobacillus brevis, Lactobacillus coleohominis, Lactobacillus crispatus, Lactobacillus crustorum, Lactobacillus curvatus, Lactobacillus diolivorans, Lactobacillus farraginis, Lactobacillus fermentum, Lactobacillus fuchuensis, Lactobacillus harbinensis, Lactobacillus helveticus, Lactobacillus hilgardii, Lactobacillus intestinalis, Lactobacillus jensenii, Lactobacillus kefiranofaciens, Lactobacillus kefiri, Lactobacillus lindneri, Lactobacillus mali, Lactobacillus manihotivorans, Lactobacillus mucosae, Lactobacillus oeni, Lactobacillus oligofermentans, Lactobacillus panis, Lactobacillus pantheris, Lactobacillus parabrevis, Lactobacillus paracollinoides, Lactobacillus parakefiri, Lactobacillus paraplantarum, Lactobacillus pentosus, Lactobacillus pontis, Lactobacillus reuteri, Lactobacillus rossiae, Lactobacillus salivarius, Lactobacillus siliginis, Lactobacillussucicola, Lactobacillus vaccinostercus, Lactobacillus vaginalis, Lactobacillus vini, Lactococcus garvieae, or Lactococcus lactis, (ii) the Faecalibacterium sp. is Faecalibacterium prausnitzii, and (iii) the Akkermansia sp. is Akkermansia. Item 2. The method of item 1, wherein (iv) the Myxococcus sp. is Myxococcus xanthus, and (v) the Pediococcus sp. is Pediococcus pentosaceus, Pediococcus acidilactici, Pediococcus damnosus, Pediococcus ethanolidurans, or Pediococcus parvulus. (Item 4) 2. The method according to item 1, wherein the Myxococcus sp. is in the form of spores, vegetative bacteria, or a mixture of spores and vegetative bacteria. (Item 5) 5. The method according to item 4, wherein the Myxococcus sp. is in the form of a powder containing spores. (Item 6) 10. The method of claim 1, wherein the subject is administered fewer than about 20, 15, 10, 9, 8, 7, or 6 different species of bacteria. (Item 7) 2. The method of claim 1, wherein the bacterial population forms part of a bacterial composition. (Item 8) 8. The method of claim 7, wherein the bacterial composition comprises less than about 20, 15, 10, 9, 8, 7, or 6 bacterial species. (Item 9) 8. The method of claim 7, wherein the bacterial composition is not a fecal transplant. (Item 10) 8. The method of claim 7, wherein the bacterial composition further comprises a pharmaceutically acceptable excipient. (Item 11) 8. The method of claim 7, wherein the bacterial composition is administered orally or rectally. (Item 12) 8. The method of claim 7, wherein the subject has an inflammatory disease. (Item 13) Item 10. The method of item 1, wherein the subject is at risk of suffering from an inflammatory disease. (Item 14) Item 15. The method of item 1, wherein the subject has at least one, two, three, or four cousins, grandparents, parents, aunts, uncles, and / or siblings who have been diagnosed with an inflammatory disease. The inflammatory disease may be any of allergies, atopy, asthma, autoimmune diseases, autoinflammatory diseases, hypersensitivity, childhood allergic asthma, allergic asthma, inflammatory bowel disease, celiac disease, Crohn's disease, colitis, ulcerative colitis, collagenous colitis, lymphocytic colitis, diverticulitis, irritable bowel syndrome, short bowel syndrome, blind loop syndrome, chronic persistent diarrhea, intractable diarrhea of ​​infancy, traveler's diarrhea, immunoproliferative small intestinal disease, chronic prostatitis, post-enteritis syndrome, tropical sprue, Whipple's disease, Wolman's disease, arthritis, rheumatoid arthritis, Behcet's disease, uveitis, pyoderma gangrenosum, erythema nodosum, and traumatic brain injury. 14. The method according to Item 13, wherein the target disease is selected from the group consisting of wounds, psoriatic arthritis, juvenile idiopathic arthritis, multiple sclerosis, systemic lupus erythematosus (SLE), myasthenia gravis, juvenile-onset diabetes, type 1 diabetes, Guillain-Barré syndrome, Hashimoto's encephalitis, Hashimoto's thyroiditis, ankylosing spondylitis, psoriasis, Sjogren's syndrome, vasculitis, glomerulonephritis, autoimmune thyroiditis, bullous pemphigoid, sarcoidosis, ichthyosis, Graves' ophthalmopathy, Addison's disease, vitiligo, acne vulgaris, pelvic inflammatory disease, reperfusion injury, sarcoidosis, graft rejection, interstitial cystitis, atherosclerosis, and atopic dermatitis. (Item 16) Item 16. The method of item 15, wherein the inflammatory disease is pediatric allergic asthma or inflammatory bowel disease. (Item 17) 10. The method of claim 1, wherein the subject is suffering from constipation, diarrhea, bloating, urinary urgency, and / or abdominal pain. (Item 18) 2. The method of claim 1, wherein the subject has received an antibiotic within the last 1, 2, 3, or 4 months. (Item 19) Item 10. The method of item 1, wherein the subject is a newborn. (Item 20) 2. The method of claim 1, wherein the subject is less than about 1, 2, 3, 4, 5, 6, 7, 8, 9, 12, 18, or 24 months of age. (Item 21) 10. The method of claim 1, wherein the subject is between about 2 and about 18 years of age, or is at least about 18 years of age. (Item 22) The subject: (a) Increased rates of Streptococcus spp., Bifidobacterium spp., and Enterococcus spp. compared with the healthy or general population; (b) reduced rates of Alternaria alternata, Aspergillus flavus, Aspergillus cibarius, and Candida sojae compared with the healthy or general population; (c) increased rates of Candida albicans and Debaryomyces spp. compared with the healthy or general population; (d) reduced rates of Bifidobacteria spp., Lactobacillus spp., Faecalibacterium spp., and Akkermansia spp. compared with the healthy or general population; (e) a reduced rate of Malassezia spp. compared with the healthy or general population; (f) an increased proportion of Bacterioides spp., Ruminococcus spp., Prevotella spp., or Bifidobacterium spp. compared with the healthy or general population; or (g) Increased rates of Enterococcus faecalis, Enterococcus faecium, or Clostridium difficile compared with the healthy or general population 2. The method according to item 1, comprising a gastrointestinal microbiome. (Item 23) The effective amount is (i) increasing the level of Bifidobacterium sp., Clostridia sp. belonging to clade IV or XIV, Lachnospira sp., and / or Ruminococcus sp. in said subject; (ii) decreasing the pH in the subject's feces; (iii) increasing the level of lactic acid in the subject's feces; (iv) increasing the level of circulating itaconate in said subject; (v) treating, reducing, or preventing allergic inflammation in a subject; (vi) reducing an adaptive immune response in the respiratory tract of said subject; (vii) reducing dendritic cell activation in gastrointestinal-associated mesenteric lymph nodes; (viii) increasing the level of reparative macrophages in the lungs, blood, serum, or plasma of said subject; (ix) increasing the level of an anti-inflammatory compound in said subject; (x) reducing the level of a pro-inflammatory compound in said subject; (xi) reducing the level of eotaxin expression and / or secretion in said subject; and / or (xii) reducing the level of mucin expression and / or secretion in said subject. Item 1, wherein the method is effective for: (Item 24) 24. The method of claim 23, wherein the effective amount is effective to reduce secretion and / or levels of mucin in the lungs of the subject. (Item 25) 24. The method of claim 23, wherein the anti-inflammatory compound is a cytokine, a microbial lipid, a microbial carbohydrate, or a microbial amino acid. (Item 26) 26. The method of claim 25, wherein the anti-inflammatory compound is IL-17. (Item 27) 24. The method of claim 23, wherein the pro-inflammatory compound is a cytokine, a microbial lipid, a microbial carbohydrate, or a microbial amino acid. (Item 28) 28. The method of claim 27, wherein the pro-inflammatory compound is IL-4, IL-10, IL-8, IL-13, TNF-α, or MUC5B. (Item 29) 10. The method of claim 1, further comprising administering to the subject (a) Bifidobacterium sp., (b) Cystobacter sp., or (c) a fungal microorganism. (Item 30) A method for treating or preventing an inflammatory disease in a subject in need thereof, comprising administering to the subject an effective amount of a bacterial population comprising Lactobacillus sp., Faecalibacterium sp., Akkermansia sp., Myxococcus sp., and Pediococcus sp. (Item 31) The inflammatory disease may be any of allergies, atopy, asthma, autoimmune diseases, autoinflammatory diseases, hypersensitivity, childhood allergic asthma, allergic asthma, inflammatory bowel disease, celiac disease, Crohn's disease, colitis, ulcerative colitis, collagenous colitis, lymphocytic colitis, diverticulitis, irritable bowel syndrome, short bowel syndrome, blind loop syndrome, chronic persistent diarrhea, intractable diarrhea of ​​infancy, traveler's diarrhea, immunoproliferative small intestinal disease, chronic prostatitis, post-enteritis syndrome, tropical sprue, Whipple's disease, Wolman's disease, arthritis, rheumatoid arthritis, Behcet's disease, uveitis, pyoderma gangrenosum, erythema nodosum, and traumatic brain injury. 31. The method according to Item 30, wherein the target disease is selected from the group consisting of wounds, psoriatic arthritis, juvenile idiopathic arthritis, multiple sclerosis, systemic lupus erythematosus (SLE), myasthenia gravis, juvenile-onset diabetes, type 1 diabetes, Guillain-Barré syndrome, Hashimoto's encephalitis, Hashimoto's thyroiditis, ankylosing spondylitis, psoriasis, Sjogren's syndrome, vasculitis, glomerulonephritis, autoimmune thyroiditis, bullous pemphigoid, sarcoidosis, ichthyosis, Graves' ophthalmopathy, Addison's disease, vitiligo, acne vulgaris, pelvic inflammatory disease, reperfusion injury, sarcoidosis, graft rejection, interstitial cystitis, atherosclerosis, and atopic dermatitis. (Item 32) A method for treating or preventing a viral respiratory infection in a subject in need thereof, comprising administering to the subject an effective amount of a bacterial population comprising Lactobacillus sp., Faecalibacterium sp., Akkermansia sp., Myxococcus sp., and Pediococcus sp. (Item 33) 33. The method of claim 32, wherein the viral respiratory infection is caused by a respiratory syncytial virus, influenza virus, parainfluenza virus, adenovirus, coronavirus, or rhinovirus. (Item 34) 33. The method of claim 32, wherein the viral respiratory infection is bronchiolitis, the common cold, croup, or pneumonia. (Item 35) A method for treating or preventing allergies in a subject in need thereof, comprising the step of administering to the subject an effective amount of a bacterial population comprising Lactobacillus sp., Faecalibacterium sp., Akkermansia sp., Myxococcus sp., and Pediococcus sp. (Item 36) 36. The method of claim 35, wherein the allergy is to milk, eggs, fish, shellfish, tree nuts, peanuts, wheat, cat, dog, or rodent dander, insect bites, pollen, latex, dust mites, or soy. (Item 37) 36. The method of claim 35, wherein the allergy is childhood allergic asthma, hay fever, or allergic airway sensitization. (Item 38) 1. A method of increasing the level of an anti-inflammatory compound and / or decreasing the level of a pro-inflammatory compound in a subject in need thereof, comprising administering to the subject an anti-inflammatory compound selected from the group consisting of Lactobacillus sp., Faecalibacterium sp., Akkermansia sp., Myxococcus sp., and Pediococcus sp. (Item 39) 39. The method of item 38, for increasing the level of the anti-inflammatory compound and / or decreasing the level of the pro-inflammatory compound in the subject's feces, blood, plasma, serum, bronchoalveolar lavage fluid, sweat, saliva, sputum, lymph, spinal fluid, urine, tears, bile, aqueous humor, vitreous humor, amniotic fluid, breast milk, cerebrospinal fluid, earwax, nasal mucus, mucus, or sebum. (Item 40) 39. The method of claim 38, wherein the anti-inflammatory compound is a microbial lipid, a microbial carbohydrate, or a microbial amino acid. (Item 41) 39. The method of claim 38, wherein the subject is suffering from a dysbiosis or an inflammatory disease. (Item 42) A composition comprising Lactobacillus sp., Faecalibacterium sp., Akkermansia sp., Myxococcus sp., and Pediococcus sp. (Item 43) Item 43. The method according to Item 42, wherein (i) the Lactobacillus sp. is Lactobacillus johnsonii, (ii) the Faecalibacterium sp. is Faecalibacterium prausnitzii, (iii) the Akkermansia sp. is Akkermansia muciniphila, (iv) the Myxococcus sp. is Myxococcus xanthus, and (v) the Pediococcus sp. is Pediococcus pentosaceus. (Item 44) 43. The composition of claim 42, comprising less than about 20, 15, 10, 9, 8, 7, or 6 different species of bacteria. (Item 45) 43. The composition of item 42, which is not a fecal transplant. (Item 46) 43. The composition of claim 42, further comprising a pharmaceutically acceptable excipient. (Item 47) 43. The composition according to item 42, which is a capsule, tablet, suspension, suppository, powder, cream, oil, oil-in-water emulsion, water-in-oil emulsion, or aqueous solution. (Item 48) 43. The composition according to item 42, in the form of a powder, solid, semi-solid, or liquid. (Item 49) a water activity (a) of less than about 0.9, 0.8, 0.7, 0.6, 0.5, 0.4, 0.3, 0.2, or 0.1 at 20°C w 43. The composition according to item 42, having (Item 50) 43. The composition according to item 42, which is a food or beverage. (Item 51) 43. The composition according to item 42, wherein the Lactobacillus sp., the Faecalibacterium sp., the Akkermansia sp., the Myxococcus sp., and / or the Pediococcus sp. is in the form of a powder. (Item 52) Item 43. The composition according to item 42, wherein the Lactobacillus sp., Faecalibacterium sp., Akkermansia sp., Myxococcus sp., and / or Pediococcus sp. are freeze-dried. (Item 53) A method for detecting a pro-inflammatory compound in a subject in need thereof, comprising: (i) obtaining a biological sample from the subject; and (ii) detecting the pro-inflammatory compound in the biological sample. (Item 54) 54. The method of item 53, wherein the subject has or is at risk of developing a dysbiosis. (Item 55) 54. The method of claim 53, wherein the subject has an inflammatory disease. (Item 56) The inflammatory disease may be any of allergies, atopy, asthma, autoimmune diseases, autoinflammatory diseases, hypersensitivity, childhood allergic asthma, allergic asthma, inflammatory bowel disease, celiac disease, Crohn's disease, colitis, ulcerative colitis, collagenous colitis, lymphocytic colitis, diverticulitis, irritable bowel syndrome, short bowel syndrome, blind loop syndrome, chronic persistent diarrhea, intractable diarrhea of ​​infancy, traveler's diarrhea, immunoproliferative small intestinal disease, chronic prostatitis, post-enteritis syndrome, tropical sprue, Whipple's disease, Wolman's disease, arthritis, rheumatoid arthritis, Behcet's disease, uveitis, pyoderma gangrenosum, erythema nodosum, and traumatic brain injury. 54. The method according to Item 53, wherein the target disease is selected from the group consisting of wounds, psoriatic arthritis, juvenile idiopathic arthritis, multiple sclerosis, systemic lupus erythematosus (SLE), myasthenia gravis, juvenile-onset diabetes, type 1 diabetes, Guillain-Barré syndrome, Hashimoto's encephalitis, Hashimoto's thyroiditis, ankylosing spondylitis, psoriasis, Sjogren's syndrome, vasculitis, glomerulonephritis, autoimmune thyroiditis, bullous pemphigoid, sarcoidosis, ichthyosis, Graves' ophthalmopathy, Addison's disease, vitiligo, acne vulgaris, pelvic inflammatory disease, reperfusion injury, sarcoidosis, graft rejection, interstitial cystitis, atherosclerosis, and atopic dermatitis. (Item 57) 54. The method of claim 53, wherein the subject is less than about 1, 2, 3, 4, 5, 6, 7, 8, 9, 12, 18, or 24 months of age. (Item 58) 54. The method of claim 53, wherein the subject is between about 2 and about 18 years of age, or is at least about 18 years of age. (Item 59) The subject: (a) Increased rates of Streptococcus spp., Bifidobacterium spp., and Enterococcus spp. compared with the healthy or general population; (b) reduced rates of Alternaria alternata, Aspergillus flavus, Aspergillus cibarius, and Candida sojae compared with the healthy or general population; (c) increased rates of Candida albicans and Debaryomyces spp. compared with the healthy or general population; (d) reduced rates of Bifidobacteria spp., Lactobacillus spp., Faecalibacterium spp., and Akkermansia spp. compared with the healthy or general population; (e) a reduced rate of Malassezia spp. compared with the healthy or general population; (f) an increased proportion of Bacterioides spp., Ruminococcus spp., Prevotella spp., or Bifidobacterium spp. compared with the healthy or general population; or (g) Increased rates of Enterococcus faecalis, Enterococcus faecium, or Clostridium difficile compared with the healthy or general population 54. The method of item 53, comprising a gastrointestinal microbiome. (Item 60) 54. The method of item 53, wherein the biological sample is a body fluid. (Item 61) 61. The method of item 60, wherein the body fluid is blood, plasma, serum, fecal water, or bronchoalveolar lavage fluid. (Item 62) Item 62. The method of item 61, wherein the bodily fluid is fecal water. (Item 63) 54. The method of claim 53, wherein the step of detecting the pro-inflammatory compound comprises contacting an antigen-presenting cell with the biological sample. (Item 64) 64. The method of item 63, wherein the antigen-presenting cells are dendritic cells. (Item 65) 54. The method of claim 53, wherein the step of detecting the proinflammatory compound further comprises contacting naive T cells with antigen-presenting cells to generate contacted T cells. (Item 66) 66. The method of item 65, further comprising detecting cytokines produced by the contacted T cells and / or progeny of the contacted T cells. (Item 67) The pro-inflammatory compound is (i) the proportion of T helper (TH)-2 cells is increased in the progeny of the contacted T cells compared to controls; (ii) the proportion of TH-1, TH-17, and / or TH22 cells is increased in the progeny of the contacted T cells compared to a control; (iii) the ratio of TH-1 cells to TH-2 cells is decreased in the progeny of the contacted T cells compared to a control; (iv) the proportion of CD8+ T cells that produce IL-17 is increased in the progeny of the contacted T cells compared to a control; and / or (v) the amount of IL-4, IL-10, and / or IL-13 produced by the progeny of the contacted T cell and / or its progeny is increased compared to a control. Item 66. The method according to Item 65, wherein the antibody is detected by (Item 68) 54. The method of claim 53, further comprising the step of instructing the subject to undergo treatment or further testing or monitoring for a dysbiosis or inflammatory disease if the pro-inflammatory compound is detected in the subject. (Item 69) 64. The method of claim 53, further comprising administering to the subject the composition of any one of claims 52 to 62 if the pro-inflammatory compound is detected in the subject. (Item 70) 54. The method of claim 53, further comprising the step of diagnosing the subject as having or at risk of developing a dysbiosis or inflammatory disease if the pro-inflammatory compound is detected in the subject. (Item 71) 81. A method for determining whether a subject has or is at risk of developing a dysbiosis or inflammatory disease, the method comprising: (i) obtaining a biological sample from the subject; and (ii) detecting a pro-inflammatory compound according to the method of any one of items 63 to 80. (Item 72) 1. A method for determining whether a subject has or is at risk of developing a dysbiosis or inflammatory disease, the method comprising: (i) obtaining a biological sample from the subject; and (ii) detecting whether the biological sample is pro-inflammatory. (Item 73) The subject: (a) Increased rates of Streptococcus spp., Bifidobacterium spp., and Enterococcus spp. compared with the healthy or general population; (b) reduced rates of Alternaria alternata, Aspergillus flavus, Aspergillus cibarius, and Candida sojae compared with the healthy or general population; (c) increased rates of Candida albicans and Debaryomyces spp. compared with the healthy or general population; (d) reduced rates of Bifidobacteria spp., Lactobacillus spp., Faecalibacterium spp., and Akkermansia spp. compared with the healthy or general population; (e) a reduced rate of Malassezia spp. compared with the healthy or general population; (f) an increased proportion of Bacterioides spp., Ruminococcus spp., Prevotella spp., or Bifidobacterium spp. compared with the healthy or general population; or (g) Increased rates of Enterococcus faecalis, Enterococcus faecium, or Clostridium difficile compared with the healthy or general population 54. The method of claim 53, further comprising determining whether the subject has a gastrointestinal microbiome. (Item 74) 72. A method of treating or preventing a dysbiosis or an inflammatory disease in a subject determined to have or be at risk of developing a dysbiosis or an inflammatory disease according to the method of item 71, comprising administering to the subject a treatment for the dysbiosis or the inflammatory disease. (Item 75) 1. A method for monitoring the effect of a treatment for a dysbiosis or inflammatory disease, the method comprising: (i) obtaining a biological sample from a subject; and (ii) detecting whether the biological sample is pro-inflammatory. (Item 76) A method for determining the activity of an inflammatory disease in a subject, the method comprising: (i) obtaining a biological sample from the subject; and (ii) detecting whether the biological sample is pro-inflammatory. (Item 77) A method for detecting an anti-inflammatory metabolite in a subject having or at risk of developing an inflammatory disease, the method comprising: (i) obtaining a biological sample from the subject; and (ii) determining the expression level of the anti-inflammatory metabolite in the biological sample. (Item 78) 1. A method for determining whether a subject has or is at risk of developing a dysbiosis or inflammatory disease, the method comprising: (i) detecting expression levels of one or more anti-inflammatory or pro-inflammatory metabolites in the subject; (ii) determining whether the expression levels are elevated or decreased compared to a standard control, wherein an elevated expression level of a pro-inflammatory metabolite or a decreased expression level of an anti-inflammatory metabolite compared to the standard control indicates that the subject has or is at risk of developing an inflammatory disease; and (iii) determining whether the subject has or is at risk of developing an inflammatory disease based at least in part on the expression levels in step (ii). (Item 79) A method for monitoring the effect of treatment on an inflammatory disease in a subject undergoing treatment for or a patient treated for an inflammatory disease, the method comprising: (i) determining a first expression level of an anti-inflammatory or pro-inflammatory metabolite in the subject at a first time point; (ii) determining a second expression level of an anti-inflammatory or pro-inflammatory metabolite in the subject at a second time point; and (iii) comparing the second expression level of an anti-inflammatory or pro-inflammatory metabolite with the first expression level of an anti-inflammatory or pro-inflammatory metabolite, thereby determining the effect of treatment on the inflammatory disease in the subject. (Item 80) A method for determining the activity of an inflammatory disease in a subject, comprising: (i) detecting the expression level of one or more anti-inflammatory or pro-inflammatory metabolites in the subject; (ii) determining whether the expression level is regulated compared to a standard control, thereby determining the activity of the inflammatory disease in the subject; and (iii) determining the activity of the inflammatory disease in the subject based at least in part on the expression level in step (ii). [Brief explanation of the drawings]

[0025] [Figure 1A]Figures 1A-1B show that significant improvement in lung histology and reduction in goblet cell hyperplasia were evident only in mice supplemented with C+Lj. Histological samples from three mice in each of the six experimental groups were stained in duplicate to visualize goblet cell hyperplasia. Figure 1A: Representative images of PAS staining for each of the six groups clearly demonstrate that mucin secretion from goblet cells (as stained) is induced in mice challenged with CRA, and that L. johnsonii and microbial consortium supplementation was the only treatment group that protected against this induction. Figure 1B: Image J was used to quantitate the percentage of PAS-stained area in each image. Each data point is represented by an individual symbol generated from two independent mouse studies. Statistical analysis of this data shows that the percentage of PAS staining associated with mice supplemented with C+Lj consortium is significantly reduced compared to all other CRA-treated groups. [Figure 1B] Figures 1A-1B show that significant improvement in lung histology and reduction in goblet cell hyperplasia were evident only in mice supplemented with C+Lj. Histological samples from three mice in each of the six experimental groups were stained in duplicate to visualize goblet cell hyperplasia. Figure 1A: Representative images of PAS staining for each of the six groups clearly demonstrate that mucin secretion from goblet cells (as stained) is induced in mice challenged with CRA, and that L. johnsonii and microbial consortium supplementation was the only treatment group that protected against this induction. Figure 1B: Image J was used to quantitate the percentage of PAS-stained area in each image. Each data point is represented by an individual symbol generated from two independent mouse studies. Statistical analysis of this data shows that the percentage of PAS staining associated with mice supplemented with C+Lj consortium is significantly reduced compared to all other CRA-treated groups.

[0026] [Figure 2]Figure 2 is a graph showing that the histological findings are supported by a significant reduction in MUC5AC expression in mice supplemented with C+Lj. RNA extracted from the lungs of each animal was used to examine gene expression levels of MUC5AC, a gene involved in mucin production by goblet cells. Data from two independent mouse studies are shown. Statistical analysis of this data indicates that the percentage of Muc5ac gene expression associated with mice supplemented with C+Lj is significantly reduced compared to all other CRA-treated groups.

[0027] [Figure 3A] Figures 3A-3C are graphs showing that C+Lj supplementation results in reduced airway expression of cytokines associated with allergic responses. Gene expression levels of several cytokines associated with allergic responses, including IL-4 (Figure 3A), IL-13 (Figure 3B), IL-10 (Figure 3C), and IL-17, were also investigated using RNA extracted from the lungs of each animal. Similarly, Applicants observed significant reductions in cytokine expression associated with C+Lj supplementation for Th2-associated cytokines (IL-4 and IL-13), as well as IL-10. Data from two independent replicates are shown. [Figure 3B] Figures 3A-3C are graphs showing that C+Lj supplementation results in reduced airway expression of cytokines associated with allergic responses. Gene expression levels of several cytokines associated with allergic responses, including IL-4 (Figure 3A), IL-13 (Figure 3B), IL-10 (Figure 3C), and IL-17, were also investigated using RNA extracted from the lungs of each animal. Similarly, Applicants observed significant reductions in cytokine expression associated with C+Lj supplementation for Th2-associated cytokines (IL-4 and IL-13), as well as IL-10. Data from two independent replicates are shown. [Figure 3C]Figures 3A-3C are graphs showing that C+Lj supplementation results in reduced airway expression of cytokines associated with allergic responses. Gene expression levels of several cytokines associated with allergic responses, including IL-4 (Figure 3A), IL-13 (Figure 3B), IL-10 (Figure 3C), and IL-17, were also investigated using RNA extracted from the lungs of each animal. Similarly, Applicants observed significant reductions in cytokine expression associated with C+Lj supplementation for Th2-associated cytokines (IL-4 and IL-13), as well as IL-10. Data from two independent replicates are shown.

[0028] [Figure 4] Figure 4 is a graph showing that the increase in the percentage of IL-17-secreting helper T cells (CD3+CD4+) was most significant in mice supplemented with C+Lj. Flow cytometry data from splenocytes reveals a significant increase in the percentage of CD4+ cells expressing IL-17, a cytokine associated with Th17 cells. This observation held true across two replicate studies, and data from both studies are shown in this figure.

[0029] [Figure 5] Figures 5A-5B are graphs showing that a bacterial consortium containing L. johnsonii but not L. rhamnosus LGG results in attenuation of allergic sensitization. CRA allergen mouse studies were performed using either L. rhamnosus LGG (LGG) or L. johnsonii (Lj) as the Lactobacillus anchor species included in the bacterial consortium supplement. To assess the effect of each consortium on sensitization, qPCR was used to determine the expression level of MUC5AC in lung tissue. While the L. johnsonii-based consortium significantly reduced MUC5AC expression, the L. rhamnosus LGG consortium failed to reduce the expression of this allergic response biomarker.

[0030] [Figure 6AB]Figures 6A-6C are graphs showing that fecal moisture from non-atopic newborns significantly reduces the expression of IL4 and IL13 responses. Figure 6A: Exposure to fecal moisture significantly reduces the number of CD4+ helper T2 cells in one donor but not both. Figure 6B: IL4 expression is significantly reduced in both donors. Figure 6C: IL13 expression is significantly reduced in both donors. [Figure 6C] Figures 6A-6C are graphs showing that fecal moisture from non-atopic newborns significantly reduces the expression of IL4 and IL13 responses. Figure 6A: Exposure to fecal moisture significantly reduces the number of CD4+ helper T2 cells in one donor but not both. Figure 6B: IL4 expression is significantly reduced in both donors. Figure 6C: IL13 expression is significantly reduced in both donors.

[0031] [Figure 7A] Figures 7A-7B are graphs showing that cell-free supernatants from distinct neonatal Candida gut microbiome isolates consistently induce CD4+IL4+ (Th2) cells (Figure 7A). Specific species induce or suppress CD4+IL10+ (T-reg) cells (Figure 7B). BHI, sterile brain-heart infusion medium exposure (control); CT, C. tropicalis; CP, C. parapsilosis; CO, C. orthopsilosis; and CT, C. tropicalis; control, non-antigen-stimulated condition; CRA, cockroach-stimulated T cells. [Figure 7B] Figures 7A-7B are graphs showing that cell-free supernatants from distinct neonatal Candida gut microbiome isolates consistently induce CD4+IL4+ (Th2) cells (Figure 7A). Specific species induce or suppress CD4+IL10+ (T-reg) cells (Figure 7B). BHI, sterile brain-heart infusion medium exposure (control); CT, C. tropicalis; CP, C. parapsilosis; CO, C. orthopsilosis; and CT, C. tropicalis; control, non-antigen-stimulated condition; CRA, cockroach-stimulated T cells.

[0032] [Figure 8A] Figures 8A-8D are graphs showing that UC microbiotypes exhibit significantly different disease severity and duration. Figure 8A: Simplified Colitis Disease Severity Score. Figure 8B: Number of extracolonic manifestations. Figure 8C: Disease duration. Figure 8D: Number of family members with inflammatory bowel disease (IBD). [Figure 8BC] Figures 8A-8D are graphs showing that UC microbiotypes exhibit significantly different disease severity and duration. Figure 8A: Simplified Colitis Disease Severity Score. Figure 8B: Number of extracolonic manifestations. Figure 8C: Disease duration. Figure 8D: Number of family members with inflammatory bowel disease (IBD). [Figure 8D] Figures 8A-8D are graphs showing that UC microbiotypes exhibit significantly different disease severity and duration. Figure 8A: Simplified Colitis Disease Severity Score. Figure 8B: Number of extracolonic manifestations. Figure 8C: Disease duration. Figure 8D: Number of family members with inflammatory bowel disease (IBD).

[0033] [Figure 9A] Figures 9A-9D are graphs showing that in vitro fecal moisture assays reveal that UC patients exhibit significantly distinct Th2 ratios, IL4 production, and CD8+IL17+ populations. Figure 9A: UC patients are characterized by a significant skewing toward Th2 responses compared to healthy controls. Figure 9B: UC microbiomes show significant differences in the degree of Th2 skewing, with the most severe microbiome (MBT-1) exhibiting the greatest Th2 skewing. Figure 9C: IL4 expression differs significantly among UC microbiomes, with the MBT-1 group exhibiting significantly higher IL4 expression compared to the least severe disease group. Figure 9D: MBT-1 patients exhibit significantly higher numbers of CD8+IL17+ cells compared to the two other less severe disease groups. [Figure 9BC]Figures 9A-9D are graphs showing that in vitro fecal moisture assays reveal that UC patients exhibit significantly distinct Th2 ratios, IL4 production, and CD8+IL17+ populations. Figure 9A: UC patients are characterized by a significant skewing toward Th2 responses compared to healthy controls. Figure 9B: UC microbiomes show significant differences in the degree of Th2 skewing, with the most severe microbiome (MBT-1) exhibiting the greatest Th2 skewing. Figure 9C: IL4 expression differs significantly among UC microbiomes, with the MBT-1 group exhibiting significantly higher IL4 expression compared to the least severe disease group. Figure 9D: MBT-1 patients exhibit significantly higher numbers of CD8+IL17+ cells compared to the two other less severe disease groups. [Figure 9D] Figures 9A-9D are graphs showing that in vitro fecal moisture assays reveal that UC patients exhibit significantly distinct Th2 ratios, IL4 production, and CD8+IL17+ populations. Figure 9A: UC patients are characterized by a significant skewing toward Th2 responses compared to healthy controls. Figure 9B: UC microbiomes show significant differences in the degree of Th2 skewing, with the most severe microbiome (MBT-1) exhibiting the greatest Th2 skewing. Figure 9C: IL4 expression differs significantly among UC microbiomes, with the MBT-1 group exhibiting significantly higher IL4 expression compared to the least severe disease group. Figure 9D: MBT-1 patients exhibit significantly higher numbers of CD8+IL17+ cells compared to the two other less severe disease groups.

[0034] [Figure 10] FIG. 10 shows an experimental timeline illustrating the schedule of phosphate-buffered saline (PBS) or therapeutic conjugate (TC) supplementation regimens and challenge with CRA in a mouse model of airway allergic sensitization.

[0035] [Figure 11]Figures 11A-11B show that oral TC supplementation of mice promotes an increase in the relative abundance of genera associated with the induction of immune tolerance. Figure 11A: Fecal microbiome composition of animals in the study was determined using 16S rRNA sequencing. Cluster analysis revealed differences in microbiome composition between treatment groups. TC-supplemented animals showed significantly distinct compositions compared to the control group. Specifically, TC-supplemented animals were enriched in species with potential immunomodulatory activity (e.g., Bifidobacterium, Clostridia species belonging to clades IV and XIV, Lachnospira, and Bacteroides). Figure 11B: Pie chart showing taxa enriched in animals treated with CRA-TC.

[0036] [Figure 12A] Figures 12A-12B show that oral TC supplementation in mice promotes metabolic reprogramming in both the intestinal lumen and periphery, including a significant increase in circulating itaconate, which is associated with a reparative macrophage effector phenotype. Figure 12A: Principal component analysis of the predominant luminal metabolites using untargeted liquid chromatography-mass spectrometry revealed distinct metabolic profiles among the three groups (Canberra distance matrix; PERMANOVA, R2 = 0.29, p = 0.005). Figure 12B: Principal component analysis of circulating metabolites identified in serum using the same strategy also revealed significant differences among the investigated groups (Canberra distance matrix; PERMANOVA, R2 = 0.29, p = 0.002). Untargeted LC-GC-mass spectrometry was used to identify and determine the relative concentrations of hundreds of metabolites in the feces (Figure 12A) and serum (Figure 12B) of mice supplemented with TC or PBS prior to challenge with cockroach (CRA) antigen. The significant spatial separation of TC-supplemented and PBS-supplemented animals in the PcoA plot indicates that the metabolite profiles in the feces and serum of these animals are significantly different. [Figure 12B]Figures 12A-12B show that oral TC supplementation in mice promotes metabolic reprogramming in both the intestinal lumen and periphery, including a significant increase in circulating itaconate, which is associated with a reparative macrophage effector phenotype. Figure 12A: Principal component analysis of the predominant luminal metabolites using untargeted liquid chromatography-mass spectrometry revealed distinct metabolic profiles among the three groups (Canberra distance matrix; PERMANOVA, R2 = 0.29, p = 0.005). Figure 12B: Principal component analysis of circulating metabolites identified in serum using the same strategy also revealed significant differences among the investigated groups (Canberra distance matrix; PERMANOVA, R2 = 0.29, p = 0.002). Untargeted LC-GC-mass spectrometry was used to identify and determine the relative concentrations of hundreds of metabolites in the feces (Figure 12A) and serum (Figure 12B) of mice supplemented with TC or PBS prior to challenge with cockroach (CRA) antigen. The significant spatial separation of TC-supplemented and PBS-supplemented animals in the PcoA plot indicates that the metabolite profiles in the feces and serum of these animals are significantly different.

[0037] [Figure 13A]Figure 13A shows histological sections of mouse airways (lungs) demonstrating that oral supplementation of mice with a metabolically active therapeutic consortium (CRA+TC) significantly reduced inflammatory influx (hematoxylin and eosin (H&E) staining; darkly stained nucleated cells) in a mouse model of airway allergic sensitization. Neither L. johnsonii alone (CRA+Lj) nor supplementing animals with four of the TC species (omitting L. johnsonii; CRA+C) conferred protection, indicating that L. johnsonii acts synergistically with the other four TC species to protect the airway mucosal surface. Heat-killed, metabolically inactive TC also did not confer protection, indicating that only metabolically active TCs confer protection. Figure 13B is a graph showing gene expression analysis of CCL-11 expression, a marker of eosinophils, confirming that the CRA+TC group exhibited a significant reduction in eosinophil presence in the lungs after allergic sensitization. [Figure 13B] Figure 13A shows histological sections of mouse airways (lungs) demonstrating that oral supplementation of mice with a metabolically active therapeutic consortium (CRA+TC) significantly reduced inflammatory influx (hematoxylin and eosin (H&E) staining; darkly stained nucleated cells) in a mouse model of airway allergic sensitization. Neither L. johnsonii alone (CRA+Lj) nor supplementing animals with four of the TC species (omitting L. johnsonii; CRA+C) conferred protection, indicating that L. johnsonii acts synergistically with the other four TC species to protect the airway mucosal surface. Heat-killed, metabolically inactive TC also did not confer protection, indicating that only metabolically active TCs confer protection. Figure 13B is a graph showing gene expression analysis of CCL-11 expression, a marker of eosinophils, confirming that the CRA+TC group exhibited a significant reduction in eosinophil presence in the lungs after allergic sensitization.

[0038] [Figure 14A]Figure 14A shows that oral supplementation of mice with a metabolically active therapeutic consortium (CRA+TC) significantly reduced mucin hypersecretion (periodic acid-Schiff (PAS) staining; dark staining) in a mouse model of airway allergic sensitization. Neither L. johnsonii alone (CRA+Lj) nor supplementing animals with four of the TC species (omitting L. johnsonii; CRA+C) reduced mucin secretion, indicating that L. johnsonii acts synergistically with the other four TC species to suppress mucin secretion at the airway mucosal surface. Heat-killed, metabolically inactive TC also did not reduce mucin secretion, indicating that only metabolically active TC conferred protection. Figure 14B is a graph showing that gene expression analysis of Muc5AC expression, a key gene involved in mucin secretion in the airways, confirms that the CRA+TC group exhibits significantly reduced mucin gene expression in the lungs compared to other treatment groups. [Figure 14B] Figure 14A shows that oral supplementation of mice with a metabolically active therapeutic consortium (CRA+TC) significantly reduced mucin hypersecretion (periodic acid-Schiff (PAS) staining; dark staining) in a mouse model of airway allergic sensitization. Neither L. johnsonii alone (CRA+Lj) nor supplementing animals with four of the TC species (omitting L. johnsonii; CRA+C) reduced mucin secretion, indicating that L. johnsonii acts synergistically with the other four TC species to suppress mucin secretion at the airway mucosal surface. Heat-killed, metabolically inactive TC also did not reduce mucin secretion, indicating that only metabolically active TC conferred protection. Figure 14B is a graph showing that gene expression analysis of Muc5AC expression, a key gene involved in mucin secretion in the airways, confirms that the CRA+TC group exhibits significantly reduced mucin gene expression in the lungs compared to other treatment groups.

[0039] [Figure 15A]Figures 15A-15C are graphs showing that oral supplementation of mice with metabolically active TC significantly reduces cytokine expression associated with allergic inflammation in a mouse model of airway allergic sensitization. Figure 15A: Boxplots demonstrating a significant decrease in the relative change in IL-13 expression in animals treated with TC and challenged with CRA compared to PBS treatment and CRA challenge. Figure 15B: Boxplots demonstrating a significant decrease in the relative change in IL-4 expression in animals treated with TC and challenged with CRA compared to PBS treatment and CRA challenge. Figure 15C: Boxplots demonstrating a significant decrease in the relative change in IL-10 expression in animals treated with TC and challenged with CRA compared to PBS treatment and CRA challenge. [Figure 15B] Figures 15A-15C are graphs showing that oral supplementation of mice with metabolically active TC significantly reduces cytokine expression associated with allergic inflammation in a mouse model of airway allergic sensitization. Figure 15A: Boxplots demonstrating a significant decrease in the relative change in IL-13 expression in animals treated with TC and challenged with CRA compared to PBS treatment and CRA challenge. Figure 15B: Boxplots demonstrating a significant decrease in the relative change in IL-4 expression in animals treated with TC and challenged with CRA compared to PBS treatment and CRA challenge. Figure 15C: Boxplots demonstrating a significant decrease in the relative change in IL-10 expression in animals treated with TC and challenged with CRA compared to PBS treatment and CRA challenge. [Figure 15C]Figures 15A-15C are graphs showing that oral supplementation of mice with metabolically active TC significantly reduces cytokine expression associated with allergic inflammation in a mouse model of airway allergic sensitization. Figure 15A: Boxplots demonstrating a significant decrease in the relative change in IL-13 expression in animals treated with TC and challenged with CRA compared to PBS treatment and CRA challenge. Figure 15B: Boxplots demonstrating a significant decrease in the relative change in IL-4 expression in animals treated with TC and challenged with CRA compared to PBS treatment and CRA challenge. Figure 15C: Boxplots demonstrating a significant decrease in the relative change in IL-10 expression in animals treated with TC and challenged with CRA compared to PBS treatment and CRA challenge.

[0040] [Figure 16AB] Figures 16A-16F are graphs showing that oral TC supplementation of mice results in a repair macrophage effector phenotype in a mouse model of airway allergic sensitization. In mice treated with CRA+TC, CD11bhiF4 / 80hi macrophages form a greater percentage of the non-lymphoid cell population in (Figure 16A) the mesenteric lymph node, (Figure 16B) the spleen, and (Figure 16C) the lung compared with animals treated with CRA+PBS. Animals treated with CRA+TC and CRA+PBS show similar percentages of CD11bhiF4 / 80hiCD206+ (M2) macrophages in the non-lymphoid cell population in both (Figure 16D) the mesenteric lymph node and (Figure 16E) the spleen. FIG. 16F: In the lungs, animals treated with CRA+TC show an increased percentage of CD11bhiF4 / 80hiCD206+ (M2) macrophages in the non-lymphocyte population compared to mice treated with CRA+PBS. [Figure 16CD]Figures 16A-16F are graphs showing that oral TC supplementation of mice results in a repair macrophage effector phenotype in a mouse model of airway allergic sensitization. In mice treated with CRA+TC, CD11bhiF4 / 80hi macrophages form a greater percentage of the non-lymphoid cell population in (Figure 16A) the mesenteric lymph node, (Figure 16B) the spleen, and (Figure 16C) the lung compared with animals treated with CRA+PBS. Animals treated with CRA+TC and CRA+PBS show similar percentages of CD11bhiF4 / 80hiCD206+ (M2) macrophages in the non-lymphoid cell population in both (Figure 16D) the mesenteric lymph node and (Figure 16E) the spleen. FIG. 16F: In the lungs, animals treated with CRA+TC show an increased percentage of CD11bhiF4 / 80hiCD206+ (M2) macrophages in the non-lymphocyte population compared to mice treated with CRA+PBS. [Figure 16EF] Figures 16A-16F are graphs showing that oral TC supplementation of mice results in a repair macrophage effector phenotype in a mouse model of airway allergic sensitization. In mice treated with CRA+TC, CD11bhiF4 / 80hi macrophages form a greater percentage of the non-lymphoid cell population in (Figure 16A) the mesenteric lymph node, (Figure 16B) the spleen, and (Figure 16C) the lung compared with animals treated with CRA+PBS. Animals treated with CRA+TC and CRA+PBS show similar percentages of CD11bhiF4 / 80hiCD206+ (M2) macrophages in the non-lymphoid cell population in both (Figure 16D) the mesenteric lymph node and (Figure 16E) the spleen. FIG. 16F: In the lungs, animals treated with CRA+TC show an increased percentage of CD11bhiF4 / 80hiCD206+ (M2) macrophages in the non-lymphocyte population compared to mice treated with CRA+PBS.

[0041] [Figure 17] FIG. 17 is a table showing the treatment groups utilized in the mouse model of airway allergic sensitization testing.

[0042] [Figure 18AB] Figures 18A-18C show that metabolic reprogramming in the intestinal lumen after oral supplementation of mice with therapeutic conjugates (TC) promotes increased concentrations of specialized lipids enriched in polyunsaturated fatty acids (PUFAs), plasmalogens. PUFAs are elevated in the feces of newborns at low risk for childhood allergies and asthma. Figure 18A: Carbohydrate compounds with decreased concentrations after treatment with TC. Figure 18B: Energy compounds with decreased concentrations after treatment with TC. Figure 18C: Lipid compounds with decreased concentrations (PUFAs, long-chain fatty acids, acylglycerols, and branched fatty acids) and increased concentrations (phospholipids and plasmalogens) after treatment with TC. [Figure 18C] Figures 18A-18C show that metabolic reprogramming in the intestinal lumen after oral supplementation of mice with therapeutic conjugates (TC) promotes increased concentrations of specialized lipids enriched in polyunsaturated fatty acids (PUFAs), plasmalogens. PUFAs are elevated in the feces of newborns at low risk for childhood allergies and asthma. Figure 18A: Carbohydrate compounds with decreased concentrations after treatment with TC. Figure 18B: Energy compounds with decreased concentrations after treatment with TC. Figure 18C: Lipid compounds with decreased concentrations (PUFAs, long-chain fatty acids, acylglycerols, and branched fatty acids) and increased concentrations (phospholipids and plasmalogens) after treatment with TC.

[0043] [Figure 19] Figure 19 is a graph showing that bacterial and fungal α-diversity and β-diversity are associated with participant age at the time of fecal sample collection. Bacterial and fungal α-diversity are inversely correlated (Shannon index; n=188; Pearson correlation, r2=-0.24; P<0.001).

[0044] [Figure 20A]Figures 20A-20B are graphs showing that the compositionally distinct, age-independent NGM status present in newborns exhibits significant differences in fungal taxonomy and is also associated with the RR of atopy at 2 years of age. Figure 20A: Ages of NGM participants did not differ significantly (n = 130; Kruskal-Wallis; P = 0.256). Boxplots are defined by the 25th and 75th percentiles. The center line represents the median (50th percentile). Whiskers are defined as the 75th percentile plus 1.5 times the interquartile range (IQR, 75-25th percentile) and the 25th percentile minus 1.5 times the interquartile range (IQR, 75-25th percentile), respectively. Figure 20B: Total allergen-specific serum IgE concentrations measured at 2 years of age (n = 130) are significantly higher in NGM3 compared to NGM1 participants (Welch t-test; P = 0.034). The box plots are constructed as defined in Figure 20A. [Figure 20B] Figures 20A-20B are graphs showing that the compositionally distinct, age-independent NGM status present in newborns exhibits significant differences in fungal taxonomy and is also associated with the RR of atopy at 2 years of age. Figure 20A: Ages of NGM participants did not differ significantly (n = 130; Kruskal-Wallis; P = 0.256). Boxplots are defined by the 25th and 75th percentiles. The center line represents the median (50th percentile). Whiskers are defined as the 75th percentile plus 1.5 times the interquartile range (IQR, 75-25th percentile) and the 25th percentile minus 1.5 times the interquartile range (IQR, 75-25th percentile), respectively. Figure 20B: Total allergen-specific serum IgE concentrations measured at 2 years of age (n = 130) are significantly higher in NGM3 compared to NGM1 participants (Welch t-test; P = 0.034). The box plots are constructed as defined in Figure 20A.

[0045] [Figure 21] Figure 21 is a graph showing that NGM shows significantly different RRs of incident PM atopy at age 2 and parent-reported physician-diagnosed asthma at age 4. The significance of risk ratios between microbiota conditions was calculated based on log-binomial regression.

[0046] [Figure 22AB]Figures 22A-22F are graphs showing that sterile fecal fluid from NGM3 participants induces dysfunction of CD4+ cell populations associated with atopic asthma. Serum-derived dendritic cells and autologous purified naive CD4+ cells from two healthy adult donors (biological replicates) were incubated with sterile fecal fluid from NGM1 participants (n=7; three biological replicates per sample) or NGM3 participants (n=5; three biological replicates per sample). Figures 22A and 22B: Fecal fluid from NGM3 participants induced a significant increase in the percentage of CD4+IL-4+ cells (LME, P<0.001; center line represents the mean) (Figure 22A) and IL-4 expression (LME; P=0.045) (Figure 22B). Figure 22C: Fecal fluid from both NGM1 and NGM3 participants induced a significant increase in the percentage of CD4+CD25+FOXP3+ cells (LME; P<0.001 for NGM1 and P=0.017 for NGM3) compared to controls. Figure 22D: Weighted correlation network analysis identified metabolic modules that distinguished NGM3 participants from NGM2 and NGM1 participants (n=28; ANOVA; P=0.038). Boxplots define the 25th and 75th percentiles; the median is represented by the centerline. The IQR (75th-25th percentile) is represented by the whiskers. Figure 22E: Scatterplot of metabolite significance against module membership (MM) for 12 metabolites in the metabolic module discriminating NGM3. Metabolites with higher metabolite significance values ​​distinguish NGM3 from other NGMs. Metabolites plotted above the dashed line (representing the overall p-value for inter-NGM differences) were significantly associated with NGM differentiation (P<0.05) and were detected at higher concentrations in NGM3 compared to the other NGMs. MM values ​​indicate the degree of inter-connectivity between a particular metabolite and other metabolites in a module (higher MM values ​​indicate greater inter-connectivity).Figure 22F: Using the same ex vivo assay as performed in Figures 22A-22C, 12,13-DiHOME significantly reduced the percentage of CD4+CD25+FOXP3+ cells at three different concentrations compared to vehicle control (LME; P=0.04, P<0.001, P=0.001 for 75, 130, and 200 μM concentrations, respectively; center line represents the mean percentage of cells). [Figure 22CD] Same as above [Figure 22EF] Same as above

[0047] [Figure 23] Figure 23 is a graph showing that a Dirichlet polynomial mixture model identifies three compositionally distinct bacterial NGMs as the best model fit. The model fit was based on a Laplace approximation to a negative logarithmic model, with lower values ​​indicating better model fit.

[0048] [Figure 24] Figure 24 is a graph showing that sterile fecal fluid from NGM3 participants induces CD4+IL-4+ cell skewing. Dendritic cells derived from serum of two healthy adult donors (biological replicates) were incubated with sterile fecal fluid from NGM1 participants (n=7; 3 biological replicates per sample) or NGM3 participants (n=5; 3 biological replicates per sample), followed by co-incubation with autologous purified naive CD4+ cells. NGM3 fecal fluid induces a trend toward CD4+IL-4+ cell skewing compared to NGM1 (LME; P=0.095).

[0049] [Figure 25]Figure 25 is a graph showing confirmation that concentrations of the dihydroxy fatty acid 12,13-DiHOME are significantly elevated in the subset of NGM3 samples used in the ex vivo assay. Using the subset of samples used in the ex vivo DC-T cell assay, the relative concentration of 12,13-DiHOME is significantly elevated in NGM3 samples (n=7) compared to NGM1 samples (n=5) based on metabolite intensity data (Welch's t-test; P=0.033).

[0050] [Figure 26] Figure 26 is a table showing the allergens used to determine the PM atopic status of the study participants, with the mean and median allergen-specific IgE (IU ml-1) for each presented.

[0051] [Figure 27] Figure 27 is a table showing the risk ratios of IGM (infants >6 months of age) for having a parent-reported incident atopy or a physician-diagnosed asthma. Risk ratios were calculated based on log-binomial regression.

[0052] [Figure 28] Figure 28 shows a table of fungal taxa showing significantly increased relative abundance in the gut microbiota of low-risk NGM1 relative to high-risk NGM3 neonates. Significant differences in relative abundance were determined using a zero-inflated negative binomial regression model (q<0.20). White background indicates taxa enriched in NGM1 (compared to NGM3), and gray background indicates taxa enriched in NGM3 (compared to NGM1). Findings are ranked by difference in relative abundance (NGM1-NGM3).

[0053] [Figure 29]Figure 29 shows a table of fungal taxa showing a significant increase in relative abundance in the gut microbiota of low-risk NGM2 relative to high-risk NGM3 neonates. Significant differences in relative abundance were determined using a zero-inflated negative binomial regression model (q<0.20). White background indicates taxa enriched in NGM2 (compared to NGM3), and gray background indicates taxa enriched in NGM3 (compared to NGM2). Findings are ranked by difference in relative abundance (NGM2-NGM3).

[0054] [Figure 30] Figure 30 is a table showing Procrustes analysis of 16S rRNA-based β-diversity, PICRUSt, and metabolomic datasets. The results of the Procrustes analysis indicate that bacterial β-diversity, PICRUSt, and metabolomic data are highly and significantly correlated.

[0055] [Figure 31A] Figures 31A-31C are graphs showing a comparison of healthy fecal microbiota (n=13) and UC-associated fecal microbiota (n=30). Figure 31A: Bacterial diversity. Horizontal bars represent the mean ± standard deviation. P values ​​were obtained by a two-tailed Student's t-test. Figure 31B: Bacterial community composition represented by non-metric multidimensional scaling (NMDS) of pairwise weighted UniFrac distances. Figure 31E: Bacterial community composition of UC patients stratified by ethnicity (18 EU UC, 12 SA UC) represented by NMDS of pairwise weighted UniFrac distances. In Figures 31B and 31E, the dashed ellipses represent the 95% confidence intervals for the centroids of each stratified group, as calculated by ordiellipse. [Figure 31BC]Figures 31A-31C are graphs showing a comparison of healthy fecal microbiota (n=13) and UC-associated fecal microbiota (n=30). Figure 31A: Bacterial diversity. Horizontal bars represent the mean ± standard deviation. P values ​​were obtained by a two-tailed Student's t-test. Figure 31B: Bacterial community composition represented by non-metric multidimensional scaling (NMDS) of pairwise weighted UniFrac distances. Figure 31E: Bacterial community composition of UC patients stratified by ethnicity (18 EU UC, 12 SA UC) represented by NMDS of pairwise weighted UniFrac distances. In Figures 31B and 31E, the dashed ellipses represent the 95% confidence intervals for the centroids of each stratified group, as calculated by ordiellipse.

[0056] [Figure 32AB] Figures 32A-32D are graphs showing clinical measures of UC severity among UC MCS (MCS1, 11 patients; MCS2, 8 patients; MCS3, 4 patients; MCS4, 3 patients). Figure 32A: Simple Clinical Colitis Activity. Figure 32B: Number of extracolonic symptoms. Figure 32C: Number of family members diagnosed with IBD. Figure 32D: Disease duration. All pairwise comparisons were performed using a two-tailed Dunn's test. Only P values ​​< 0.1 are shown. EU UC, squares; SA UC, circles. [Figure 32CD] Figures 32A-32D are graphs showing clinical measures of UC severity among UC MCS (MCS1, 11 patients; MCS2, 8 patients; MCS3, 4 patients; MCS4, 3 patients). Figure 32A: Simple Clinical Colitis Activity. Figure 32B: Number of extracolonic symptoms. Figure 32C: Number of family members diagnosed with IBD. Figure 32D: Disease duration. All pairwise comparisons were performed using a two-tailed Dunn's test. Only P values ​​< 0.1 are shown. EU UC, squares; SA UC, circles.

[0057] [Figure 33AB]Figures 33A-33K are graphs showing in vitro human T cell activity after coculture with autologous DCs co-incubated with sterile fecal fluid. Figure 33A: Th1 to Th2 ratio; Figure 33B: Th1 frequency; Figure 33C: Th2 frequency; Figure 33D: Th17 frequency; e, frequency of regulatory T cells (48 healthy individuals, 16 UC1 individuals). Comparisons of Th1 frequency (Figure 33F), Th2 frequency (Figure 33G), and Th1 to Th2 ratio (Figure 33H) between healthy and UC MCS are shown (48 healthy individuals, 48 ​​MCS1, 40 MCS2, 16 MCS3, and 8 MCS4 individuals). The concentrations of IL-4 (Figure 33I), IL-5 (Figure 33J), and IL-13 (Figure 33K) in cell supernatants are shown after coculture of human T cells with autologous DCs challenged with sterile fecal fluid from healthy participants and MCS1 and MCS2 patients (48 healthy participants, 48 ​​MCS1 patients, and 40 MCS2 patients). Data were generated from four replicate experiments (Figures 33A-33H) or two replicate experiments (Figures 33I-33K) using DC / T cells obtained from two anonymous PBMC donors. Bars (mean fit values ​​for each group) and P values ​​were determined by linear mixed-effects modeling (see Materials and Methods). P values ​​<0.1 are indicated. [Figure 33CD] Same as above [Figure 33EF] Same as above [Figure 33GH] Same as above [Figure 33IJ] Same as above [Figure 33K] Same as above

[0058] [Figure 34A]Figures 34A-34H show graphs comparing healthy fecal fungal microbiota (n = 13) with fecal fungal microbiota associated with UC (n = 30). Figure 34A: Fungal α-diversity stratified by health status. Figure 34B: Fungal community composition represented by NMDS of pairwise Bray-Curtis distances. Participants are colored by health status. Bacterial α-diversity (Figure 34C) and fungal α-diversity (Figure 34D) were stratified by health status and ethnicity (healthy EU, 10 patients; healthy SA, 3 patients; UC EU, 18 patients; UC SA, 12 patients). Figure 34E: Simplified clinical colitis activity in UC patients stratified by ethnicity (EU UC, 14 patients; SA UC, 12 patients). P values ​​were obtained by a two-tailed rank-sum test. Figure 34F: Bacterial community composition of all participants stratified by ethnicity (EU, 28 participants, SA, 15 participants) as represented by NMDS of pairwise weighted UniFrac distances. Figure 34G: Fungal community composition of all participants stratified by ethnicity (EU, 28 participants, SA, 15 participants) as represented by NMDS of pairwise Bray-Curtis distances. Figure 34H: Bacterial community composition profiled by PhyloChip of UC patients stratified by ethnicity (EU UC, 15 participants, SA UC, 11 participants) as represented by NMDS of pairwise Canberra distances. In panels a, c, and d, horizontal bars represent the mean ± standard deviation. P values ​​were obtained by two-tailed t-test. In Figure 34B and Figures 34F–34H, dashed ellipses represent the 95% confidence intervals for the centroids of each participant stratification group calculated by ordiellipse. Each dot / square represents a single stool sample obtained from a single donor. [Figure 34BC] Same as above [Figure 34DE] Same as above [Figure 34FG] Same as above [Figure 34H] Same as above

[0059] [Figure 35]Figures 35A-35B show the bacterial community composition of UC patients stratified by UC MCS. Figure 35A: NMDS of pairwise weighted UniFrac distances for 16S rRNA profiles obtained by Illumina MiSeq (MCS1, 12 patients; MCS2, 10 patients; MCS3, 4 patients; MCS4, 3 patients; other, 1 patient). Figure 35B: NMDS of pairwise Canberra distances for 16S rRNA profiles obtained by PhyloChip (MCS1, 10 patients; MCS2, 8 patients; MCS3, 4 patients; MCS4, 2 patients; other, 1 patient). Dashed ellipses represent the 95% confidence intervals for the centroids of each participant stratification group calculated by ordiellipse. Each dot / square represents a single fecal sample obtained from a single donor.

[0060] [Figure 36] Figure 36 is a graph showing in vitro human T cell activity after co-culture with autologous DCs co-incubated with sterile fecal moisture. The induced Th1 to Th2 ratios are compared for EU UC patients (n=) and SA UC patients. Data were generated from four replicate experiments using DC / T cells obtained from two anonymous PBMC donors. Bars (mean fit values ​​for each group) and P values ​​were determined by linear mixed-effects modeling.

[0061] [Figure 37] Figure 37 is a table showing the breakdown of the study participant cohort. Note: Gender could not be reported for one SA-UC participant.

[0062] [Figure 38] Figure 38 is a table describing the Metabolon QC samples.

[0063] [Figure 39] FIG. 39 is a table showing Metabolon QC standards. DETAILED DESCRIPTION OF THE INVENTION

[0064] I. Definition While various embodiments and aspects of the present invention have been shown and described herein, it will be apparent to those skilled in the art that such embodiments and aspects are presented by way of example only. Numerous variations, changes, and substitutions will readily occur to those skilled in the art without departing from the invention. It should be understood that various alternatives to the embodiments of the invention described herein can be employed in practicing the invention.

[0065] The section headings used herein are for organizational purposes only and are not to be construed as limiting the subject matter described. All documents or portions of documents cited in this application, including, without limitation, patents, patent applications, papers, books, manuals, and treatises, are hereby expressly incorporated by reference in their entirety for all purposes.

[0066] Unless otherwise defined, technical and scientific terms used herein have the same meaning as those commonly understood by those skilled in the art.For example, see Singleton et al., DICTIONARY OF MICROBIOLOGY AND MOLECULAR BIOLOGY, 2nd edition, J. Wiley & Sons (New York, NY 1994); Sambrook et al., MOLECULAR CLONING, A LABORATORY MANUAL, Cold Springs Harbor Press (Cold Springs Harbor, NY 1989).Any method, device and material similar or equivalent to those described herein can be used in the practice of the present invention.The following definitions are provided to facilitate understanding of certain terms frequently used herein, and do not limit the scope of this disclosure.

[0067] The term "exogenous" refers to a molecule or substance (e.g., a compound, nucleic acid, or protein) that originates from outside a given cell or organism. For example, an "exogenous promoter," as referred to herein, is a promoter that does not originate from the plant that expresses it. Conversely, the terms "endogenous" or "endogenous promoter" refer to a molecule or substance that is native to or originates within a given cell or organism.

[0068] The term "isolated," when applied to a nucleic acid or protein, indicates that the nucleic acid or protein is essentially free from other cellular components with which it is naturally associated. It can be, for example, in a homogeneous state, and can be in a dry or aqueous solution. Purity and homogeneity are generally determined using analytical chemistry techniques such as polyacrylamide gel electrophoresis or high performance liquid chromatography. A protein that is the predominant species present in a preparation is substantially purified.

[0069] The term "isolated," as applied to bacteria, refers to bacteria that (1) have been separated from at least some of the components with which they were associated when originally produced (whether in nature or in a laboratory setting) and / or (2) have been produced, prepared, purified, and / or manufactured by the hand of man using artificial culture conditions, such as (but not limited to) culture on plates and / or in a fermenter. Isolated bacteria include bacteria that have been cultured, even if such culture is not a monoculture. Isolated bacteria can be separated from at least about 10%, about 20%, about 30%, about 40%, about 50%, about 60%, about 70%, about 80%, about 90%, or more of the other components with which they were originally associated. In embodiments, the isolated bacteria are greater than about 80%, about 85%, about 90%, about 91%, about 92%, about 93%, about 94%, about 95%, about 96%, about 97%, about 98%, about 99%, or greater than about 99% pure. In embodiments, the bacterial populations provided herein comprise isolated bacteria. In embodiments, the compositions provided herein comprise isolated bacteria. In embodiments, the administered bacteria are isolated bacteria.

[0070] As used herein, a substance is "pure" if it is substantially free of other components. The terms "purify," "purifying," and "purified," when applied to bacteria, refer to bacteria that have been separated from at least some of the components that accompanied it when it was originally produced or developed (e.g., whether in nature or in an experimental setting), or any time after it was originally produced. A bacterium or bacterial population can be considered purified if it has been isolated at the time of production or thereafter, for example, from a material or environment containing the bacterium or bacterial population, or by culture passaging; a purified bacterium or bacterial population may contain up to about 10%, 20%, 30%, 40%, 50%, 60%, 70%, 80%, 90%, or more than about 90% other materials and still be considered "isolated." In some embodiments, purified bacteria and bacterial populations are greater than about 80%, about 85%, about 90%, about 91%, about 92%, about 93%, about 94%, about 95%, about 96%, about 97%, about 98%, about 99%, or greater than about 99% pure. In the case of the microbial compositions provided herein, one or more bacterial types (species or strains) present in the composition can be purified independently from one or more other bacteria produced and / or present in the material or environment containing the bacterial type. Microbial compositions and their bacterial components are generally purified from the products of their remaining habitat.

[0071] The terms "polypeptide," "peptide," and "protein" are used interchangeably herein to refer to a polymer of amino acid residues, which, in embodiments, may be conjugated to a moiety that is not composed of amino acids. These terms apply to amino acid polymers in which one or more amino acid residues are artificial chemical mimetics of corresponding naturally occurring amino acids, as well as to naturally occurring and non-naturally occurring amino acid polymers. A "fusion protein" refers to a chimeric protein encoding two or more separate protein sequences that are recombinantly expressed as a single moiety.

[0072] The terms "peptidyl" and "peptidyl moiety" refer to a monovalent peptide.

[0073] The term "amino acid" refers to naturally occurring and synthetic amino acids, as well as amino acid analogs and amino acid mimetics that function in a manner similar to naturally occurring amino acids. Naturally occurring amino acids are those encoded by the genetic code, as well as those that have been later modified, such as hydroxyproline, γ-carboxyglutamate, and O-phosphoserine. Amino acid analogs refer to compounds that have the same basic chemical structure as a naturally occurring amino acid, i.e., an α-carbon bonded to a hydrogen, a carboxyl group, an amino group, and an R group, such as homoserine, norleucine, methionine sulfoxide, and methionine methylsulfonium. Such analogs have modified R groups (e.g., norleucine) or modified peptide backbones, but retain the same basic chemical structure as naturally occurring amino acids. Amino acid mimetics refer to chemical compounds that have a structure different from the general chemical structure of an amino acid but function in a manner similar to a naturally occurring amino acid. The terms "non-naturally occurring amino acid" and "unnatural amino acid" refer to amino acid analogs, synthetic amino acids, and amino acid mimetics that are not found in nature.

[0074] Amino acids may be referred to herein by either their commonly known three letter symbols or by the one-letter symbols recommended by the IUPAC-IUB Biochemical Nomenclature Commission. Similarly, nucleotides may be referred to by their commonly accepted single-letter codes.

[0075] "Conservatively modified variants" applies to both amino acid and nucleic acid sequences. With respect to a particular nucleic acid sequence, "conservatively modified variants" refers to nucleic acids that encode identical or essentially identical amino acid sequences. Due to the degeneracy of the genetic code, several nucleic acid sequences encode any given protein. For example, the codons GCA, GCC, GCG, and GCU all encode the amino acid alanine. Thus, at every position where alanine is specified by a codon, the codon can be altered to any of the corresponding codons described without altering the encoded polypeptide. Such nucleic acid variations are "silent variations," which are one species of conservatively modified variations. Every nucleic acid sequence herein that encodes a polypeptide also describes every possible silent variation of the nucleic acid. Those skilled in the art will recognize that each codon in a nucleic acid (except AUG, which is normally the only codon for methionine, and TGG, which is normally the only codon for tryptophan) can be altered to obtain a functionally identical molecule. Thus, every described sequence implicitly encompasses every silent variation of a nucleic acid that encodes a polypeptide.

[0076] With respect to amino acid sequences, those skilled in the art will recognize that individual substitutions, deletions, or additions to nucleic acid, peptide, polypeptide, or protein sequences that alter, add, or delete a single amino acid or a small percentage of amino acids in the encoded sequence are "conservatively modified variants," in which the resulting amino acid is replaced with a chemically similar amino acid. Conservative substitution tables providing functionally similar amino acids are well known in the art. Such conservatively modified variants are in addition to, and do not exclude, polymorphic variants, interspecies homologs, and alleles of the invention.

[0077] The following eight groups each contain amino acids that are conservative substitutions for one another: 1) Alanine (A), Glycine (G); 2) aspartic acid (D), glutamic acid (E); 3) asparagine (N), glutamine (Q); 4) arginine (R), lysine (K); 5) isoleucine (I), leucine (L), methionine (M), valine (V); 6) phenylalanine (F), tyrosine (Y), tryptophan (W); 7) serine (S), threonine (T); and 8) Cysteine ​​(C), Methionine (M) (See, for example, Creighton, Proteins (1984)).

[0078] The term "identical" or percent "identity" refers to two or more sequences or subsequences that, in the case of two or more nucleic acid or polypeptide sequences, have the same or a specified percentage of identical amino acid residues or nucleotides (i.e., about 60% identity over a specified region when compared and aligned for maximum correspondence over a comparison window or specified region, preferably 65%, 70%, 75%, 80%, 85%, 90%, 91%, 92%, 93%, 94%, 95%, 96%, 97%, 98%, 99%, or higher identity) as measured using the BLAST or BLAST 2.0 sequence comparison algorithm with the default parameters described below, or by manual alignment and visual inspection (see, for example, the NCBI website http: / / www.ncbi.nlm.nih.gov / BLAST / ). Such sequences are then said to be "substantially identical." This definition also refers to or can apply to the complement of a test sequence. This definition also includes sequences that have deletions and / or additions, as well as sequences that have substitutions. As described below, preferred algorithms can account for gaps, etc. Preferably, identity exists over a region that is at least about 25 amino acids or nucleotides in length, or more preferably over a region that is 50-100 amino acids or nucleotides in length.

[0079] A "label" or "detectable moiety" is a composition that can be detected by spectroscopic, photochemical, biochemical, immunochemical, chemical, or other physical means. For example, useful labels include 32P, fluorescent dyes (e.g., cyanines), electron-dense reagents, enzymes (e.g., as commonly used in ELISA), biotin, digoxigenin, or haptens and proteins, or other entities that can be made detectable, for example, by incorporating a radiolabel into a peptide or antibody that specifically reacts with a target peptide. Any suitable method known in the art for conjugating an antibody to a label can be used, for example, the method described in Hermanson, Bioconjugate Techniques, 1996, Academic Press, Inc., San Diego.

[0080] "Contacting" is used according to its simple and ordinary meaning to refer to the process of bringing at least two distinct species (e.g., chemical compounds, including biomolecules, and / or cells, such as bacterial cells) into sufficient proximity to react, interact, or physically touch. However, it should be understood that the resulting reaction product can be produced directly from the reaction between the added reagents or from intermediates derived from one or more of the added reagents that may occur in the reaction mixture.

[0081] The term "contacting" can include reacting, interacting, or physically touching two species, where the two species can be, for example, an antibody domain and an antibody binding domain described herein. In embodiments, contacting includes, for example, allowing an antibody domain described herein to interact with an antibody binding domain.

[0082] A "patient" or "subject in need thereof" refers to a living member of the animal kingdom who is afflicted with or susceptible to the indicated disorder. In embodiments, the subject is a member of a species that includes individuals who naturally suffer from the disease. In embodiments, the subject is a mammal. Non-limiting examples of mammals include rodents (e.g., mice and rats), primates (e.g., lemurs, galagos, monkeys, apes, and humans), rabbits, dogs (e.g., companion dogs, service dogs, or working dogs such as police dogs, military dogs, racing dogs, or ornamental dogs), horses (e.g., race horses and working horses), cats (e.g., domestic cats), livestock (e.g., pigs, cows, donkeys, mules, bison, goats, camels, and sheep), and deer. In embodiments, the subject is a human. In embodiments, the subject is a non-mammalian animal, such as a turkey, duck, or chicken. In embodiments, a subject is a living organism suffering from or susceptible to a disease or condition that can be treated by administering a composition or pharmaceutical composition presented herein.

[0083] The term "disease" or "condition" refers to the state of existence or health of a patient or subject that can be treated using the compounds, pharmaceutical compositions, or methods presented herein. In embodiments, the disease is an inflammatory disease (e.g., asthma, ulcerative colitis, irritable bowel syndrome, arthritis, uveitis, pyoderma gangrenosum, erythema nodosum, or any other inflammatory disease mentioned herein). As used herein, a "symptom" of a disease includes any clinical or laboratory manifestation associated with the disease, and is not limited to what a subject can feel or notice.

[0084] As used herein, the term "inflammatory disease" refers to a disease or condition characterized by abnormal inflammation (e.g., elevated levels of inflammation compared to a control, such as a healthy person, without the disease). Non-limiting examples of inflammatory diseases include allergies, atopy, asthma, autoimmune diseases, autoinflammatory diseases, hypersensitivity, childhood allergic asthma, allergic asthma, inflammatory bowel disease, celiac disease, Crohn's disease, colitis, ulcerative colitis, collagenous colitis, lymphocytic colitis, diverticulitis, irritable bowel syndrome, short bowel syndrome, blind loop syndrome, chronic persistent diarrhea, intractable diarrhea of ​​infancy, traveler's diarrhea, immunoproliferative small bowel disease, chronic prostatitis, postenteritis syndrome, tropical sprue, Whipple's disease, Wolman's disease, arthritis, rheumatoid arthritis, Behcet's disease, uveitis, pyoderma gangrenosum, nodular ulcerative colitis, and inflammatory bowel disease. These include erythema, traumatic brain injury, psoriatic arthritis, juvenile idiopathic arthritis, multiple sclerosis, systemic lupus erythematosus (SLE), myasthenia gravis, juvenile-onset diabetes, type 1 diabetes, Guillain-Barré syndrome, Hashimoto's encephalitis, Hashimoto's thyroiditis, ankylosing spondylitis, psoriasis, Sjögren's syndrome, vasculitis, glomerulonephritis, autoimmune thyroiditis, bullous pemphigoid, sarcoidosis, ichthyosis, Graves' ophthalmopathy, Addison's disease, vitiligo, acne vulgaris, pelvic inflammatory disease, reperfusion injury, sarcoidosis, graft rejection, interstitial cystitis, atherosclerosis, and atopic dermatitis.

[0085] As used herein, the term "dysbiosis" refers to differences in the gastrointestinal microbiota compared to a healthy or general population. In embodiments, dysbiosis includes differences in the commensal species diversity of the gastrointestinal microbiota compared to a healthy or general population. In some embodiments, dysbiosis includes a decrease in beneficial microorganisms and / or an increase in pathobionts (pathogenic or potentially pathogenic microorganisms) and / or a decrease in the overall microbiota species diversity. Many factors, including, but not limited to, antibiotic use, psychological and physical stress, radiation, and dietary changes, can harm beneficial members of the gut microbiota, thereby resulting in dysbiosis. In some embodiments, dysbiosis includes or promotes the overgrowth of bacterial opportunistic pathogens, such as Enterococcus faecalis, Enterococcus faecium, or Clostridium difficile. In certain embodiments, dysbiosis comprises a reduction (e.g., a 5%, 10%, 15%, 20%, 25%, 30%, 35%, 40%, 45%, 50%, 55%, 60%, 65%, 70%, 75%, 80%, 85%, 90%, 95% or greater reduction) in the amount (absolute number or percentage of the total microbial population) of bacterial or fungal cells of a species or genus compared to a healthy subject (e.g., a corresponding subject without an inflammatory disease, infection, and a corresponding subject who has not received an antibiotic within about 1, 2, 3, 4, 5, or 6 months, and / or compared to a healthy or general population). In some embodiments, dysbiosis comprises an increase (e.g., a 5%, 10%, 15%, 20%, 25%, 30%, 35%, 40%, 45%, 50%, 55%, 60%, 65%, 70%, 75%, 80%, 85%, 90%, 95% or greater increase) in the amount (absolute number or percentage of the total microbial population) of bacterial or fungal cells within a species or genus compared to healthy subjects (e.g., compared to corresponding subjects without inflammatory disease, infection, and corresponding subjects who have not received an antibiotic within about 1, 2, 3, 4, 5, or 6 months, and / or compared to the healthy or general population).In some embodiments, a subject with gastrointestinal infection, gastrointestinal inflammation, diarrhea, colitis, or who has received antibiotics within about 1, 2, 3, 4, 5, 6, 7, 8, 9, or 10 weeks is considered to have dysbiosis. In some embodiments, the impaired microbiota includes bacterial or fungal overgrowth in the small intestine. The administration of antibiotics (e.g., systemically, e.g., by intravenous injection, or orally) is a common and significant cause of significant changes in the normal microbiota. Therefore, as used herein, the term "antibiotic-induced dysbiosis" refers to dysbiosis caused by or following the administration of antibiotics.

[0086] Non-limiting examples of dysbiosis are described in the examples presented herein. Non-limiting examples of dysbiosis associated with neonates are also described in Fujimura et al. (2016) "Neonatal gut microbiota associates with childhood multisensitized atopy and T cell differentiation," Nature Medicine, 22(10):1187-1191 (hereinafter "Fujimura et al., 2016"), the entire contents of which (including all supplementary information and data) are incorporated herein by reference. In some embodiments, the subject with dysbiosis has the NGM3 microbiome profile described in Fujimura et al., 2016. Non-limiting examples of dysbiosis associated with ulcerative colitis are described in Mar et al. (2016) "Disease Severity and Immune Activity "Relate to Distinct Interkingdom Gut Microbiome States in Ethnically Distinct Ulcerative Colitis Patients," mBio 7(4):e01072-16 (hereinafter "Mar et al., 2016"). In some embodiments, a subject with dysbiosis has an MCS4 microbiome profile as described in Mar et al., 2016. In some embodiments, a subject with dysbiosis has an MCS3 microbiome profile as described in Mar et al., 2016. In some embodiments, a subject with dysbiosis has an MCS2 microbiome profile as described in Mar et al., 2016. In some embodiments, a subject with dysbiosis has an MCS1 microbiome profile as described in Mar et al., 2016.

[0087] The term "associated" or "associated with," with respect to a substance or the activity or function of a substance associated with a disease (e.g., allergy, asthma, ulcerative colitis, irritable bowel syndrome, arthritis, uveitis, pyoderma gangrenosum, or erythema nodosum), means that the disease is caused (in whole or in part) by the substance or the activity or function of the substance, or that the symptoms of the disease are caused (in whole or in part) by the substance or the activity or function of the substance.

[0088] The term "abnormal" as used herein refers to something different from normal. When used to describe enzyme activity, abnormal refers to activity that is higher or lower than the average of normal control or normal non-disease control samples. Abnormal activity can refer to an amount of activity that causes disease, where restoring the abnormal activity to a normal amount or an amount that is not associated with disease (for example, by using the methods described herein) results in a reduction of the disease or one or more disease symptoms.

[0089] A "control" or "standard control" refers to a reference, usually a known reference, for comparison with a test sample, measurement, or value. For example, a test sample can be obtained from a patient suspected of having a given disease (e.g., dysbiosis, autoimmune disease, inflammatory autoimmune disease, cancer, infectious disease, immune disease, or other disease) and compared to a known normal (non-disease) individual (e.g., a standard control subject). A standard control can also represent an average measurement or value collected from similar individuals (e.g., standard control subjects) who do not have a given disease, e.g., a population of healthy individuals with a similar medical background, the same age, weight, etc. (i.e., a standard control population). A standard control value can also be obtained from the same individual, e.g., from a sample previously obtained from the patient before the onset of the disease. For example, a control can be designed to compare therapeutic benefit based on pharmacological data (e.g., half-life) or therapeutic metrics (e.g., comparison of side effects). Controls are also useful for determining the significance of data. For example, if the values ​​for a given parameter vary widely in the controls, the variation in the test sample is not considered significant. Those skilled in the art will recognize that standard controls can be designed to evaluate any number of parameters (e.g., microbiome, RNA levels, protein levels, specific cell types, specific body fluids, specific tissues, synovial cells, synovial fluid, synovial tissue, fibroblast-like synoviocytes, macrophage-like synoviocytes, etc.).

[0090] Those skilled in the art will understand which standard control is most appropriate in a given situation, and can analyze data based on comparison with standard control values.Standard control is also useful for determining the significance (e.g., statistical significance) of data.For example, if the value of a given parameter varies widely in standard control, the variation in test sample will not be considered significant.

[0091] The term "diagnosis" refers to the relative probability of the presence of a disease (e.g., an autoimmune disease, an inflammatory autoimmune disease, a cancer disease, an infectious disease, an immune disease, or other disease) in a subject. Similarly, the term "prognosis" refers to the relative probability that a certain future outcome with respect to a pathological condition will occur in a subject. For example, in the context of the present invention, prognosis can refer to the likelihood that an individual will develop a disease (e.g., an autoimmune disease, an inflammatory autoimmune disease, a cancer disease, an infectious disease, an immune disease, or other disease), or the likely severity of the disease (e.g., the duration of the disease). The terms are not absolute, as will be understood by anyone skilled in the art of medical diagnostics.

[0092] "Biological sample" or "sample" refers to a material obtained or derived from a subject or patient. Biological samples include sections of tissue, such as biopsy and autopsy samples, obtained for histological purposes, and frozen sections. Such samples include bodily fluids, such as blood and blood fractions or products (e.g., serum, plasma, platelets, red blood cells, etc.), feces and fecal fractions or products (e.g., fecal water, including, but not limited to, fecal water separated from other fecal components and solids by methods such as centrifugation and filtration), sputum, tissue, cultured cells (e.g., primary cultures, explants, and transformed cells), stool, urine, synovial fluid, joint tissue, synovial tissue, synovial cells, fibroblast-like synoviocytes, macrophage-like synoviocytes, immune cells, hematopoietic cells, fibroblasts, macrophages, dendritic cells, T cells, and the like. In some embodiments, the sample is obtained from a eukaryote, e.g., a mammal, e.g., a primate such as a chimpanzee or a human; a cow; a dog; a cat; a rodent, e.g., a guinea pig, a rat, a mouse; a rabbit; or a bird; a reptile; or a fish.

[0093] As used herein, "cell" refers to a cell that performs metabolic or other functions sufficient to preserve or replicate its genomic DNA. Cells can be identified by methods well known in the art, including, for example, the presence of an intact membrane, staining with a specific dye, the ability to produce progeny, or, in the case of gametes, the ability to combine with a second gamete to produce viable offspring. Cells can include prokaryotic and eukaryotic cells. Prokaryotic cells include, but are not limited to, bacteria. Eukaryotic cells include, but are not limited to, yeast cells and cells derived from plants and animals, such as mammalian, insect (e.g., Spodoptera) and human cells. Cells can be useful if they are naturally non-adherent or have been treated, for example, by trypsinization, to prevent them from adhering to surfaces.

[0094] As used herein, the abbreviation "sp." for species refers to at least one species (e.g., 1, 2, 3, 4, 5, or more species) of the indicated genus. The abbreviation "spp." for species refers to two or more species (e.g., 2, 3, 4, 5, 6, 7, 8, 9, 10, or more) of the indicated genus. In embodiments, the methods and compositions provided herein include a single species within the indicated genus(s) or two or more (e.g., a plurality including more than two) species within the indicated genus(s). In embodiments, one, two, three, four, five, or more or all of the indicated species are isolated. In embodiments, the indicated species are administered together. In embodiments, each of the indicated species is present in a single composition comprising each of the species. In multiple embodiments, each of the species is administered simultaneously, for example, within about 1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 30, or 60, 1-5, 1-10, 1-30, 1-60, or 5-15 seconds of each other or within about 1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 30, or 60, 1-5, 1-10, 1-30, 1-60, or 5-15 minutes of each other.

[0095] In this disclosure, "comprises," "comprising," "containing," and "having," etc., may have the meaning ascribed to them in U.S. Patent Law and may mean "includes," "including," etc. "Consisting essentially of" or "consists essentially" similarly have the meaning ascribed to them in U.S. Patent Law and are open-ended, permitting the presence of more than what is recited, but excluding prior art embodiments, so long as the basic or novel characteristics of the recited items are not altered by the presence of more than what is recited. In contrast, the transitional phrase "consisting of" excludes any unspecified element, step, or ingredient.

[0096] As used herein, the term "about," with respect to a numerical value or range, means ±10% of the recited or claimed numerical value or range, unless a more restrictive range is required by context.

[0097] In the specification and claims, the terms "at least one of" or "one or more of" are used interchangeably. Phrases such as "(more of)" may be present, followed by a conjunction list of elements or features. The term "and / or" may also be present in a list of two or more elements or features. Unless otherwise implicitly or explicitly contradicted by the context in which it is used, such a phrase shall mean any of the listed elements or features individually, or any of the listed elements or features in combination with any of the other listed elements or features. For example, the phrases "at least one of A and B"; "one or more of A and B"; and "A and / or B" shall mean "A only, B only, or A and B," respectively. A similar interpretation is intended with respect to lists containing three or more items. For example, the phrases "at least one of A, B, and C"; "one or more of A, B, and C"; and "A, B, and / or C" shall mean "A only, B only, C only, A and B, A and C, B and C, or A, B, and C," respectively. Furthermore, use of the term "based on" above and in the claims is intended to mean "based at least in part on," and thus allows for unrecited features or elements.

[0098] When a range of a parameter is provided, it is understood that all integers and tenths thereof within that range are also provided by the present invention. For example, "0.2 to 5 mg" is a disclosure of 0.2 mg, 0.3 mg, 0.4 mg, 0.5 mg, 0.6 mg, etc., up to and including 5.0 mg.

[0099] As used in this description and throughout the claims that follow, the meanings of "a," "an," and "the" include plural references unless the context clearly dictates otherwise. II. Bacterial Populations and Microbial Composition

[0100] In some aspects, the composition comprises a bacterial population comprising, consisting essentially of, or consisting of 1, 2, 3, 4, 5, 6, 7, or 8 (or at least 1, 2, 3, 4, 5, 6, 7, or 8) bacterial species. In some embodiments, the bacterial population comprises Lactobacillus sp., Faecalibacterium sp., Akkermansia The bacterial population comprises, consists essentially of, or consists of any one, two, three, four, five, six, seven, or eight of Lactobacillus sp., Myxococcus sp., Cystobacter sp., Pediococcus sp., Bifidobacterium sp., and Clostridium sp. In embodiments, the bacterial population comprises Lactobacillus sp. and Faecalibacterium prausnitzii. In embodiments, the bacterial population comprises Lactobacillus sp. and Akkermansia muciniphila. In embodiments, the bacterial population comprises Lactobacillus sp. and Myxococcus xanthus. In embodiments, the bacterial population comprises Lactobacillus sp. and Cystobacter fuscus. In some embodiments, the bacterial population comprises a Lactobacillus sp. and Pediococcus pentosaceus, Pediococcus acidilactici, Pediococcus damnosus, Pediococcus ethanolidurans, or Pediococcus parvulus. In some embodiments, the bacterial population comprises a Lactobacillus sp. and Bifidobacterium bifidum, Bifidobacterium pseudolongum, Bifidobacterium saeculare, or Bifidobacterium subtile. In some embodiments, the bacterial population comprises a Lactobacillus sp. and Clostridium hiranonis.In some embodiments, Lactobacillus sp. is Lactobacillus johnsonii, Lactobacillus rhamnosus, Lactobacillus zeae, Lactobacillus acidipiscis, Lactobacillus acidophilus, Lactobacillus agilis, Lactobacillus aviarius, Lactobacillus brevis, Lactobacillus coleohominis, Lactobacillus crispatus, Lactobacillus crustorum, Lactobacillus curvatus, Lactobacillus diolivorans, Lactobacillus farraginis, Lactobacillus fermentum, Lactobacillus fuchuensis, Lactobacillus harbinensis, Lactobacillus helveticus, Lactobacillus hilgardii, Lactobacillus intestinalis, Lactobacillus jensenii, Lactobacillus kefiranofaciens, Lactobacillus kefiri, Lactobacillus lindneri, Lactobacillus mali, Lactobacillus manihotivorans, Lactobacillus mucosae, Lactobacillus oeni, Lactobacillus oligofermentans, Lactobacillus panis, Lactobacillus pantheris, Lactobacillus parabrevis, Lactobacillus. paracollinoides, Lactobacillus parakefiri, Lactobacillus paraplantarum, Lactobacillus pentosus, Lactobacillus pontis, Lactobacillus reuteri, Lactobacillus rossiae, Lactobacillus salivarius, Lactobacillus siliginis, Lactobacillus sucicola, Lactobacillus vaccinostercus, Lactobacillus vaginalis, Lactobacillus vini, Lactococcus garvieae or Lactococcus lactis. In some embodiments, the Lactobacillus sp. is Lactobacillus johnsonii. In some embodiments, the bacterial population is: Lactobacillus johnsonii, Lactobacillus rhamnosus, Lactobacillus zeae, Lactobacillus acidipiscis, Lactobacillus acidophilus, Lactobacillus agilis, Lactobacillus aviarius, Lactobacillus brevis, Lactobacillus coleohominis, Lactobacillus crispatus, Lactobacillus crustorum, Lactobacillus curvatus, Lactobacillus diolivorans, Lactobacillus farraginis, Lactobacillus fermentum, Lactobacillus fuchuensis, Lactobacillus harbinensis, Lactobacillus helveticus, Lactobacillus hilgardii、Lactobacillus intestinalis、Lactobacillus jensenii、Lactobacillus kefiranofaciens、Lactobacillus kefiri、Lactobacilluslindneri, Lactobacillus mali, Lactobacillus manihotivorans, Lactobacillus mucosae, Lactobacillus oeni, Lactobacillus oligofermentans, Lactobacillus panis, Lactobacillus pantheris, Lactobacillus parabrevis, Lactobacillus paracollinoides, Lactobacillus parakefiri, Lactobacillus paraplantarum, Lactobacillus pentosus, Lactobacillus pontis, Lactobacillus reuteri, Lactobacillus rossiae, Lactobacillus salivarius, Lactobacillus siliginis, Lactobacillus sucicola, Lactobacillus vaccinostercus, Lactobacillus vaginalis, Lactobacillus vini, Lactococcus In some embodiments, the bacterial population comprises at least 1, 2, 3, 4, 5, 6, 7, 8, 9, or 10, or 1-5, 1-10, 1-5, or 1-20 of any combination of Lactobacillus johnsonii, Faecalibacterium prausnitzii, Akkermansia muciniphila, Myxococcus xanthus, Cystobacter fuscus, Pediococcus pentosaceus, Pediococcus acidilactici, Pediococcus damnosus, Pediococcus ethanolidurans, and Pediococcus parvulus. In some embodiments, the bacterial population comprises Lactobacillus johnsonii, Faecalibacterium prausnitzii, Akkermansia muciniphila, Myxococcus xanthus, and / or Pediococcus pentosaceus. In some embodiments, the bacterium is an isolated bacterium.

[0101] In some aspects, compositions are provided that include a Lactobacillus sp., a Faecalibacterium sp., an Akkermansia sp., a Myxococcus sp., and / or a Pediococcus sp. In embodiments, (i) the Lactobacillus sp. is Lactobacillus johnsonii, (ii) the Faecalibacterium sp. is Faecalibacterium prausnitzii, (iii) the Akkermansia sp. is Akkermansia muciniphila, (iv) the Myxococcus sp. is Myxococcus xanthus, and (v) the Pediococcus sp. is Pediococcus pentosaceus.

[0102] In some aspects, a composition is provided comprising a Lactobacillus sp., a Faecalibacterium sp., an Akkermansia sp., a Cystobacter sp., and a Pediococcus sp. In embodiments, (i) the Lactobacillus sp. is Lactobacillus johnsonii, (ii) the Faecalibacterium sp. is Faecalibacterium prausnitzii, (iii) the Akkermansia sp. is Akkermansia muciniphila, (iv) the Cystobacter sp. is Cystobacter fuscus, and (v) the Pediococcus sp. is Pediococcus pentosaceus.

[0103] In embodiments, the bacterial population further comprises Bifidobacterium sp. or Clostridium sp. In embodiments, the Bifidobacterium sp. is Bifidobacterium bifidum, Bifidobacterium pseudolongum, Bifidobacterium saeculare, or Bifidobacterium subtile. In embodiments, the Clostridium sp. is Clostridium hiranonis.

[0104] In one embodiment, a microbial composition is provided, the composition comprising Lactobacillus johnsonii, Faecalibacterium prausnitzii, Akkermansia muciniphila, Myxococcus xanthus, Pediococcus pentosaceus, and a biological carrier suitable for enteral administration.

[0105] In one embodiment, a microbial composition is provided, the composition comprising Lactobacillus johnsonii, Faecalibacterium prausnitzii, Akkermansia muciniphila, Myxococcus xanthus, or Pediococcus pentosaceus and a biological carrier suitable for enteral administration.

[0106] In embodiments, the biological carrier is suitable for oral or rectal administration. In embodiments, the biological carrier is suitable for intestinal colonization. As referred to herein, a "biologically acceptable" (or "pharmacologically acceptable") carrier refers to molecular entities and compositions described herein that do not produce adverse allergic or other untoward reactions when administered to an animal or human.

[0107] In embodiments, the composition comprises fewer than about 20, 19, 18, 17, 16, 15, 14, 13, 12, 11, 10, 9, 8, 7, 6, 5, 4, 3, or 2 different species of bacteria. In embodiments, the composition comprises fewer than about 20 different species of bacteria. In embodiments, the composition comprises fewer than 20 different species of bacteria. In embodiments, the composition comprises fewer than about 15 different species of bacteria. In embodiments, the composition comprises fewer than 15 different species of bacteria. In embodiments, the composition comprises fewer than 15 different species of bacteria. In embodiments, the composition comprises fewer than 10 different species of bacteria. In embodiments, the composition comprises fewer than 10 different species of bacteria. In embodiments, the composition comprises fewer than about 9 different species of bacteria. In embodiments, the composition comprises fewer than 9 different species of bacteria. In embodiments, the composition comprises fewer than 8 different species of bacteria. In embodiments, the composition comprises fewer than 8 different species of bacteria. In embodiments, the composition comprises fewer than 7 different species of bacteria. In embodiments, the composition comprises fewer than 7 different species of bacteria. In embodiments, the composition comprises fewer than about 6 different species of bacteria. In embodiments, the composition comprises fewer than 6 different species of bacteria. In embodiments, the composition comprises fewer than about 5 different species of bacteria. In embodiments, the composition comprises fewer than 5 different species of bacteria. In embodiments, the composition comprises fewer than about 4 different species of bacteria. In embodiments, the composition comprises fewer than 4 different species of bacteria. In embodiments, the composition comprises fewer than about 3 different species of bacteria. In embodiments, the composition comprises fewer than 3 different species of bacteria. In embodiments, the composition comprises fewer than about 2 different species of bacteria. In embodiments, the composition comprises fewer than 2 different species of bacteria.

[0108] In some embodiments, the composition is not a fecal transplant. In some embodiments, the composition further comprises a pharmaceutically acceptable excipient. In some embodiments, the composition is a capsule, tablet, suspension, suppository, powder, cream, oil, oil-in-water emulsion, water-in-oil emulsion, or aqueous solution. In some embodiments, the composition is in the form of a powder, solid, semi-solid, or liquid. In some embodiments, the composition is a food or beverage.

[0109] In embodiments, the Lactobacillus sp., Faecalibacterium sp., Akkermansia sp., Myxococcus sp., and / or Pediococcus sp. are in powder form. In embodiments, the Lactobacillus sp., Faecalibacterium sp., Akkermansia sp., Myxococcus sp., and / or Pediococcus sp. are lyophilized.

[0110] In embodiments, the Myxococcus sp. is in the form of spores, vegetative bacteria, or a mixture of spores and vegetative bacteria. In embodiments, the Myxococcus sp. is in the form of a powder containing spores. In embodiments, the Clostridium sp. is in the form of spores, vegetative bacteria, or a mixture of spores and vegetative bacteria. In embodiments, the Clostridium sp. is in the form of a powder containing spores.

[0111] In embodiments, the bacterial composition has a water activity (a) at 20° C. of less than about 0.9, 0.8, 0.7, 0.6, 0.5, 0.4, 0.3, 0.2, or 0.1. w In some embodiments, the bacterial composition has an a of less than about 0.9 at 20°C. w In embodiments, the bacterial composition has an a of less than 0.9 at 20°C. w In embodiments, the bacterial composition has an a of less than about 0.8 at 20°C. wIn some embodiments, the bacterial composition has an a of less than 0.8 at 20°C. w In embodiments, the bacterial composition has an a of less than about 0.7 at 20°C. w In embodiments, the bacterial composition has an a of less than 0.7 at 20°C. w In embodiments, the bacterial composition has an a of less than about 0.6 at 20°C. w In some embodiments, the bacterial composition has an a of less than 0.6 at 20°C. w In embodiments, the bacterial composition has an a of less than about 0.5 at 20°C. w In embodiments, the bacterial composition has an a of less than 0.5 at 20°C. w In embodiments, the bacterial composition has an a of less than about 0.4 at 20°C. w In some embodiments, the bacterial composition has an a of less than 0.4 at 20°C. w In embodiments, the bacterial composition has an a of less than about 0.3 at 20°C. w In some embodiments, the bacterial composition has an a of less than 0.3 at 20°C. w In embodiments, the bacterial composition has an a of less than about 0.2 at 20°C. w In embodiments, the bacterial composition has an a of less than 0.2 at 20°C. w In embodiments, the bacterial composition has an a of less than about 0.1 at 20°C. w In some embodiments, the bacterial composition has an a of less than 0.1 at 20°C. w It has.

[0112] As provided herein, a "microbial composition" refers to a composition comprising a bacterial population comprising, consisting essentially of, or consisting of any one, two, three, four, five, six, seven, or eight of Lactobacillus sp., Faecalibacterium sp., Akkermansia sp., Myxococcus sp., Cystobacter sp., Pediococcus sp., Bifidobacterium sp., and Clostridium sp. In embodiments, the bacterial population comprises Lactobacillus sp. and Faecalibacterium prausnitzii. In embodiments, the bacterial population comprises Lactobacillus sp. and Faecalibacterium prausnitzii. In embodiments, the bacterial population comprises Lactobacillus sp. and Faecalibacterium prausnitzii. In some embodiments, the bacterial population includes Lactobacillus sp. and Myxococcus xanthus. In embodiments, the bacterial population includes Lactobacillus sp. and Cystobacter fuscus. In embodiments, the bacterial population includes Lactobacillus sp. and Pediococcus pentosaceus, Pediococcus acidilactici, Pediococcus damnosus, Pediococcus ethanolidurans, or Pediococcus parvulus. In embodiments, the bacterial population includes Lactobacillus sp. and Bifidobacterium bifidum, Bifidobacterium pseudolongum, Bifidobacterium saeculare, or Bifidobacterium subtile. In embodiments, the bacterial population includes Lactobacillus sp. and Clostridium hiranonis. In embodiments, Lactobacillus sp. is Lactobacillus johnsonii, Lactobacillus rhamnosus, Lactobacillus zeae, Lactobacillus acidipiscis, Lactobacillus acidophilus, Lactobacillus agilis, Lactobacillus aviarius, Lactobacillus brevis, Lactobacillus coleohominis, Lactobacillus crispatus, Lactobacillus crustorum, Lactobacillus curvatus, Lactobacillus diolivorans, Lactobacillus farraginis, Lactobacillus fermentum, Lactobacillus fuchuensis, Lactobacillus harbinensis, Lactobacillus helveticus, Lactobacillus hilgardii, Lactobacillus intestinalis, Lactobacillus jensenii, Lactobacillus kefiranofaciens, Lactobacillus kefiri, Lactobacillus lindneri, Lactobacillus mali, Lactobacillus manihotivorans, Lactobacillus mucosae, Lactobacillus oeni, Lactobacillus oligofermentans, Lactobacillus panis, Lactobacillus pantheris, Lactobacillus parabrevis, Lactobacillus paracollinoides, Lactobacillus parakefiri, Lactobacillus paraplantarum, Lactobacillus pentosus, Lactobacillus pontis, Lactobacillus reuteri, Lactobacillus rossiae, Lactobacillus salivarius, Lactobacillus siliginis, Lactobacillus sucicola, Lactobacillus vaccinostercus, Lactobacillus vaginalis, Lactobacillus vini, Lactococcus garvieae or Lactobacillus lactis. In multiple embodiments, Lactobacillus sp. agilis, Lactobacillus aviarius, Lactobacillus brevis, Lactobacillus coleohominis, Lactobacillus crispatus, Lactobacillus crustorum, Lactobacillus curvatus, Lactobacillus diolivorans, Lactobacillus farraginis, Lactobacillus fermentum, Lactobacillus fuchuensis, Lactobacillus harbinensis, Lactobacillus helveticus, Lactobacillus hilgardii, Lactobacillus intestinalis, Lactobacillus jensenii, Lactobacillus kefiranofaciens, Lactobacillus kefiri, Lactobacillus lindneri, Lactobacillus mali, Lactobacillus manihotivorans, Lactobacillus mucosae, Lactobacillus oeni, Lactobacillus oligofermentans, Lactobacillus panis, Lactobacillus pantheris, Lactobacillus parabrevis, Lactobacillus paracollinoides, Lactobacillus parakefiri, Lactobacillus paraplantarum, Lactobacillus pentosus, Lactobacillus pontis, Lactobacillus reuteri, Lactobacillus rossiae, Lactobacillus salivarius, Lactobacillus siliginis, Lactobacillus sucicola, Lactobacillus vaccinostercus, Lactobacillus vaginalis, Lactobacillus vini, Lactococcus garvieae, Lactococcus lactis, Faecalibacterium prausnitzii, Akkermansia muciniphila, Myxococcus xanthus, Cystobacter fuscus, Pediococcus pentosaceus, Pediococcus acidilactici, Pediococcus damnosus, Pediococcus ethanolidurans and Pediococcus In some embodiments, the microbial composition comprises at least 1, 2, 3, 4, 5, 6, 7, 8, 9, or 10, or 1-5, 1-10, 1-5, or 1-20 of any combination of Lactobacillus johnsonii, Faecalibacterium prausnitzii, Akkermansia muciniphila, Myxococcus xanthus, and / or Pediococcus pentosaceus. In some embodiments, the microbial composition comprises bacterial cells of one or more of the bacterial species Lactobacillus johnsonii, Faecalibacterium prausnitzii, Akkermansia muciniphila, Myxococcus xanthus, or Pediococcus pentosaceus.In embodiments, the composition comprises Lactobacillus johnsonii, Faecalibacterium prausnitzii, Akkermansia muciniphila, Myxococcus xanthus, and Pediococcus pentosaceus. In embodiments, the composition comprises Lactobacillus johnsonii, Faecalibacterium prausnitzii, Akkermansia muciniphila, Myxococcus xanthus, or Pediococcus. pentosaceus. In some embodiments, the bacterium is isolated. As used herein, a "type" or more than one "type" of bacteria can be distinguished at the genus level, species level, subspecies level, strain level, or by any other taxonomic method described herein or otherwise known in the art.

[0113] In some embodiments, the composition comprises an effective amount of Lactobacillus johnsonii, Faecalibacterium prausnitzii, Akkermansia muciniphila, Myxococcus xanthus, and Pediococcus pentosaceus. In some embodiments, the composition comprises an effective amount of Lactobacillus johnsonii, Faecalibacterium prausnitzii, Akkermansia muciniphila, Myxococcus xanthus, or Pediococcus pentosaceus. In some embodiments, the composition consists essentially of an effective amount of Lactobacillus johnsonii, Faecalibacterium prausnitzii, Akkermansia muciniphila, Myxococcus xanthus, and Pediococcus pentosaceus. In embodiments, the composition comprises an effective amount of Lactobacillus johnsonii, Faecalibacterium prausnitzii, Akkermansia muciniphila, Myxococcus xanthus, and Pediococcus pentosaceus. When a microbial composition "consists essentially of" Lactobacillus johnsonii, Faecalibacterium prausnitzii, Akkermansia muciniphila, Myxococcus xanthus, and Pediococcus pentosaceus, other agents that do not interfere with the operation or the basic and novel properties of the microbial composition may be included.

[0114] An "effective amount" is an amount sufficient to achieve a stated purpose (e.g., achieve the effect for which it is administered, treat a disease, reduce enzyme activity, or alleviate one or more symptoms of a disease or condition). An example of an "effective amount" is an amount sufficient to contribute to the treatment, prevention, or alleviation of a symptom or symptoms of a disease, which may also be referred to as a "therapeutically effective amount." Thus, an "effective amount" or "therapeutically effective amount" as provided herein refers to the amount of a bacterial population (e.g., a bacterial population comprising one or more species or strains of bacteria, e.g., a bacterial population comprising Lactobacillus johnsonii, Faecalibacterium prausnitzii, Akkermansia muciniphila, Myxococcus xanthus, and / or Pediococcus pentosaceus) required to improve or prevent the symptoms of a disease (e.g., a dysbiosis, an infectious disease, or an inflammatory disease) compared to an untreated patient. In some embodiments, the microbial composition does not include Lactobacillus rhamnosus.

[0115] "Alleviating" a symptom(s) (and grammatical equivalents of this phrase) means reducing the severity or frequency of the symptom(s), or eliminating the symptom(s). A "prophylactically effective amount" of a drug is an amount of drug that, when administered to a subject, has the intended prophylactic effect, e.g., prevents or delays the onset (or recurrence) of an injury, disease, symptom, or condition, or reduces the likelihood of the onset (or recurrence) of a disease, symptom, or condition, or its symptoms. A complete prophylactic effect does not necessarily occur with the administration of a single dose, but may occur only after the administration of a series of doses. Thus, a prophylactically effective amount can be administered in one or more administrations. "An activity-reducing amount," as used herein, refers to the amount of an antagonist required to reduce the activity of an enzyme or protein compared to the absence of the antagonist. "A function-disrupting amount," as used herein, refers to the amount of an antagonist required to disrupt the function of an enzyme or protein compared to the absence of the antagonist. Guidance can be found in the literature regarding appropriate dosages for a given class of pharmaceutical product. For example, for a given parameter, an effective amount will represent an increase or decrease of at least 5%, 10%, 15%, 20%, 25%, 40%, 50%, 60%, 75%, 80%, 90%, or at least 100%. Efficacy can also be expressed as a "-fold" increase or decrease. For example, a therapeutically effective amount may have an effect that is at least 1.2-fold, 1.5-fold, 2-fold, 5-fold, or greater than the control. The exact amount will depend on the purpose of the treatment and can be ascertained by one of ordinary skill in the art using known techniques (see, e.g., Lieberman, Pharmaceutical Dosage Forms (Vols. 1-3, 1992); Lloyd, The Art, Science and Technology of Pharmaceutical Compounding (1999); Pickar, Dosage Calculations (1999); and Remington: The Science and Practice of Pharmacy, 20th ed., 2003, Gennaro, Ed., Lippincott, Williams & Wilkins).

[0116] In embodiments, the compositions provided herein can be administered orally and are 3 From 10 15 In some embodiments, the composition contains up to 10 colony forming units (cfu) / g of live microorganisms. 4 ~10 15 In some embodiments, the composition comprises 10 5 ~10 15 In some embodiments, the composition comprises 10 6 ~10 15 In some embodiments, the composition comprises 10 7 ~10 15 In some embodiments, the composition comprises 10 8 ~10 15 In some embodiments, the composition comprises 10 9 ~10 15 In some embodiments, the composition comprises 10 10 ~10 15 In some embodiments, the composition comprises 10 11 ~10 15 In some embodiments, the composition comprises 10 12 ~10 15 In some embodiments, the composition comprises 10 13 ~10 15 In some embodiments, the composition comprises 10 14 ~10 15 In some embodiments, the composition comprises 10 3 From 10 15 In some embodiments, the composition contains up to 10 4 ~10 15 In some embodiments, the composition comprises 10 5 ~10 15In some embodiments, the composition comprises 10 6 ~10 15 In some embodiments, the composition comprises 10 7 ~10 15 In some embodiments, the composition comprises 10 8 ~10 15 In some embodiments, the composition comprises 10 9 ~10 15 In some embodiments, the composition comprises 10 10 ~10 15 In some embodiments, the composition comprises 10 11 ~10 15 In some embodiments, the composition comprises 10 12 ~10 15 In some embodiments, the composition comprises 10 13 ~10 15 In some embodiments, the composition comprises 10 14 ~10 15 Contains cfu.

[0117] In embodiments, the compositions provided herein can be administered orally and are 3 From 10 14 In some embodiments, the composition contains up to 10 colony forming units (cfu) / g of live microorganisms. 4 ~10 14 In some embodiments, the composition comprises 10 5 ~10 14 In some embodiments, the composition comprises 10 6 ~10 14 In some embodiments, the composition comprises 10 7 ~10 14 In some embodiments, the composition comprises 10 8 ~10 14 In some embodiments, the composition comprises 10 9 ~10 14 In some embodiments, the composition comprises 10 10 ~10 14In some embodiments, the composition comprises 10 11 ~10 14 In some embodiments, the composition comprises 10 12 ~10 14 In some embodiments, the composition comprises 10 13 ~10 14 In some embodiments, the composition comprises 10 3 From 10 14 In some embodiments, the composition contains up to 10 4 ~10 14 In some embodiments, the composition comprises 10 5 ~10 14 In some embodiments, the composition comprises 10 6 ~10 14 In some embodiments, the composition comprises 10 7 ~10 14 In some embodiments, the composition comprises 10 8 ~10 14 In some embodiments, the composition comprises 10 9 ~10 14 In some embodiments, the composition comprises 10 10 ~10 14 In some embodiments, the composition comprises 10 11 ~10 14 In some embodiments, the composition comprises 10 12 ~10 14 In some embodiments, the composition comprises 10 13 ~10 14 Contains cfu.

[0118] In embodiments, the compositions provided herein can be administered orally and are 3 From 10 13 In some embodiments, the composition contains up to 10 colony forming units (cfu) / g of live microorganisms. 4 ~10 13 In some embodiments, the composition comprises 10 5 ~10 13In some embodiments, the composition comprises 10 6 ~10 13 In some embodiments, the composition comprises 10 7 ~10 13 In some embodiments, the composition comprises 10 8 ~10 13 In some embodiments, the composition comprises 10 9 ~10 13 In some embodiments, the composition comprises 10 10 ~10 13 In some embodiments, the composition comprises 10 11 ~10 13 In some embodiments, the composition comprises 10 12 ~10 13 In some embodiments, the composition comprises 10 3 From 10 13 In some embodiments, the composition contains up to 10 4 ~10 13 In some embodiments, the composition comprises 10 5 ~10 13 In some embodiments, the composition comprises 10 6 ~10 13 In some embodiments, the composition comprises 10 7 ~10 13 In some embodiments, the composition comprises 10 8 ~10 13 In some embodiments, the composition comprises 10 9 ~10 13 In some embodiments, the composition comprises 10 10 ~10 13 In some embodiments, the composition comprises 10 11 ~10 13 In some embodiments, the composition comprises 10 12 ~10 13 Contains cfu.

[0119] In embodiments, the compositions provided herein can be administered orally and are 3 From 10 12 In some embodiments, the composition contains up to 10 colony forming units (cfu) / g of live microorganisms. 4 ~10 12 In some embodiments, the composition comprises 10 5 ~10 12 In some embodiments, the composition comprises 10 6 ~10 12 In some embodiments, the composition comprises 10 7 ~10 12 In some embodiments, the composition comprises 10 8 ~10 12 In some embodiments, the composition comprises 10 9 ~10 12 In some embodiments, the composition comprises 10 10 ~10 12 In some embodiments, the composition comprises 10 11 ~10 12 In some embodiments, the composition comprises 10 3 From 10 12 In some embodiments, the composition contains up to 10 4 ~10 12 In some embodiments, the composition comprises 10 5 ~10 12 In some embodiments, the composition comprises 10 6 ~10 12 In some embodiments, the composition comprises 10 7 ~10 12 In some embodiments, the composition comprises 10 8 ~10 12 In some embodiments, the composition comprises 10 9 ~10 12 In some embodiments, the composition comprises 10 10 ~10 12 In some embodiments, the composition comprises 10 11~10 12 Contains cfu.

[0120] In embodiments, the compositions provided herein can be administered orally and are 3 From 10 11 In some embodiments, the composition contains up to 10 colony forming units (cfu) / g of live microorganisms. 4 ~10 11 In some embodiments, the composition comprises 10 5 ~10 11 In some embodiments, the composition comprises 10 6 ~10 11 In some embodiments, the composition comprises 10 7 ~10 11 In some embodiments, the composition comprises 10 8 ~10 11 In some embodiments, the composition comprises 10 9 ~10 11 In some embodiments, the composition comprises 10 3 From 10 11 In some embodiments, the composition contains up to 10 4 ~10 11 In some embodiments, the composition comprises 10 5 ~10 11 In some embodiments, the composition comprises 10 6 ~10 11 In some embodiments, the composition comprises 10 7 ~10 11 In some embodiments, the composition comprises 10 8 ~10 11 In some embodiments, the composition comprises 10 9 ~10 11 Contains cfu.

[0121] In embodiments, the compositions provided herein can be administered orally and are 3 From 10 10In some embodiments, the composition contains up to 10 colony forming units (cfu) / g of live microorganisms. 4 ~10 10 In some embodiments, the composition comprises 10 5 ~10 10 In some embodiments, the composition comprises 10 6 ~10 10 In some embodiments, the composition comprises 10 7 ~10 10 In some embodiments, the composition comprises 10 8 ~10 10 In some embodiments, the composition comprises 10 9 ~10 10 In some embodiments, the composition comprises 10 3 From 10 10 In some embodiments, the composition contains up to 10 4 ~10 10 In some embodiments, the composition comprises 10 5 ~10 10 In some embodiments, the composition comprises 10 6 ~10 10 In some embodiments, the composition comprises 10 7 ~10 10 In some embodiments, the composition comprises 10 8 ~10 10 In some embodiments, the composition comprises 10 9 ~10 10 Contains cfu.

[0122] In embodiments, the compositions provided herein can be administered orally and are 3 From 10 9 In some embodiments, the composition contains up to 10 colony forming units (cfu) / g of live microorganisms. 4 ~10 9 In some embodiments, the composition comprises 10 5 ~10 9 In some embodiments, the composition comprises 106 ~10 9 In some embodiments, the composition comprises 10 7 ~10 9 In some embodiments, the composition comprises 10 8 ~10 9 In some embodiments, the composition comprises 10 3 From 10 9 In some embodiments, the composition contains up to 10 4 ~10 9 In some embodiments, the composition comprises 10 5 ~10 9 In some embodiments, the composition comprises 10 6 ~10 9 In some embodiments, the composition comprises 10 7 ~10 9 In some embodiments, the composition comprises 10 8 ~10 9 Contains cfu.

[0123] In embodiments, the compositions provided herein can be administered orally and are 3 From 10 8 In some embodiments, the composition contains up to 10 colony forming units (cfu) / g of live microorganisms. 4 ~10 8 In some embodiments, the composition comprises 10 5 ~10 8 In some embodiments, the composition comprises 10 6 ~10 8 In some embodiments, the composition comprises 10 7 ~10 8 In some embodiments, the composition comprises 10 3 From 10 8 In some embodiments, the composition contains up to 10 4 ~10 8 In some embodiments, the composition comprises 10 5 ~10 8In some embodiments, the composition comprises 10 6 ~10 8 In some embodiments, the composition comprises 10 7 ~10 8 Contains cfu.

[0124] In embodiments, the compositions provided herein can be administered orally and are 3 From 10 7 In some embodiments, the composition contains up to 10 colony forming units (cfu) / g of live microorganisms. 4 ~10 7 In some embodiments, the composition comprises 10 5 ~10 7 In some embodiments, the composition comprises 10 6 ~10 7 In some embodiments, the composition comprises 10 3 From 10 7 In some embodiments, the composition contains up to 10 4 ~10 7 In some embodiments, the composition comprises 10 5 ~10 7 In some embodiments, the composition comprises 10 6 ~10 7 Contains cfu.

[0125] It is understood that the amounts of colony forming units (cfu) / g and cfu provided herein may refer to the amount of each bacterial species strain administered (individually), or may refer to the total cfu / g or cfu for the bacterial population.

[0126] The proportion or concentration of the composition of the present invention in a pharmaceutical composition can vary depending on several factors, including dosage, chemical properties (e.g., hydrophobicity), and route of administration. For example, a defined microbial composition can be provided in a capsule containing from about 0.005 mg to about 1000 mg for oral administration. Alternatively, or in addition, the dosage can be expressed as cfu or cfu / g of bacteria as described above (e.g., dry weight when expressed as cfu / g). In some embodiments, the dosage can vary, but is preferably about 10 2 ~about 10 15 cfu / g, e.g., 1xl0 2 cfu / g, 5xl0 2 cfu / g, 1xl0 3 cfu / g, 5xl0 3 cfu / g, 1xl0 4 cfu / g, 5xl0 4 cfu / g, 1xl0 5 cfu / g, 5xl0 5 cfu / g, 1xl0 6 cfu / g, 5xl0 6 cfu / g, 1xl0 7 cfu / g, 5xl0 7 cfu / g, 1xl0 8 cfu / g, 5xl0 8 cfu / g, 1xl0 9 cfu / g, 5xl0 9 cfu / g, 1xl0 10 cfu / g, 5xl0 10 cfu / g, lxl0 11 cfu / g, 5xl0 11 cfu / g or 1xl0 12 In some embodiments, Lactobacillus johnsonii, Faecalibacterium prausnitzii, Akkermansia muciniphila, Myxococcus xanthus, or Pediococcus pentosaceus may be present in an amount ranging from 10 to 1000 cfu / g dry weight. 3 , 10 4 , 10 5 , 10 6 , 10 7 , 108 , 10 9 , 10 10 , 10 11 , 10 12 , 10 13 , 10 14 or 10 15 In some embodiments, the composition is administered at about 10 colony forming units (cfu) / g dry weight, or total cfu. 7 colony forming units (cfu) / g or total 10 7 In some embodiments, the composition comprises about 10 cfu of Lactobacillus johnsonii. 7 colony forming units (cfu) / g or total 10 7 cfu Akkermansia In some embodiments, the composition comprises about 10 7 colony forming units (cfu) / g or total 10 7 In some embodiments, the composition comprises about 10 cfu of Myxococcus xanthus. 7 colony forming units (cfu) / g or total 10 7 In some embodiments, the composition comprises about 10 cfu of Pediococcus pentosaceus. 8 colony forming units (cfu) / g or total 10 8 cfu of Faecalibacterium prausnitzii. In embodiments, the composition comprises live microorganisms (e.g., Lactobacillus johnsonii, Faecalibacterium prausnitzii, Akkermansia muciniphila, Myxococcus xanthus, or Pediococcus pentosaceus) per gram of composition, or an equivalent dose calculated for inactivated or dead microorganisms, for microbial fractions, or for metabolic products produced.

[0127] In some embodiments, the Lactobacillus johnsonii provided herein refers to one or more isolated bacterial cells of strains cultured from mouse intestines using Lactobacillus isolation media (deMan, Rogose, and Sharpe agar). Non-limiting examples of Lactobacillus johnsonii include strains deposited with the ATCC under accession numbers 11506 and 53672.

[0128] In embodiments, Lactobacillus rhamnosus as provided herein refers to one or more isolated bacterial cells of a bacterial strain having all of the identifying characteristics of the strain deposited with ATCC under accession number 53103; a variant of the strain deposited with ATCC under accession number 53103 having all of the identifying characteristics of the strain ATCC under accession number 53103; and a variant of the strain deposited with ATCC under accession number 53103 having all of the identifying characteristics of the strain ATCC under accession number 53103.

[0129] In embodiments, Faecalibacterium prausnitzii as provided herein refers to one or more isolated bacterial cells of a bacterial strain having all of the identifying characteristics of the strain deposited with ATCC under accession number 27766; a variant of the strain deposited with ATCC under accession number 27766 having all of the identifying characteristics of strain ATCC under accession number 27766; and a variant of the strain deposited with ATCC under accession number 27766 having all of the identifying characteristics of strain ATCC under accession number 27766.

[0130] In embodiments, Akkermansia muciniphila as provided herein refers to one or more isolated bacterial cells of the bacterial strain having all of the identifying characteristics of the strain deposited with the ATCC under accession number BAA-835; a variant of the strain deposited with the ATCC under accession number BAA-835 having all of the identifying characteristics of the strain ATCC under accession number BAA-835; and a variant of the strain deposited with the ATCC under accession number BAA-835 having all of the identifying characteristics of the strain ATCC under accession number BAA-835.

[0131] In embodiments, Myxococcus xanthus as provided herein refers to one or more isolated bacterial cells of the bacterial strain having all of the identifying characteristics of the strain deposited with ATCC under accession number 25232; a variant of the strain deposited with ATCC under accession number 25232 having all of the identifying characteristics of the strain ATCC under accession number 25232; and a variant of the strain deposited with ATCC under accession number 25232 having all of the identifying characteristics of the strain ATCC under accession number 25232.

[0132] In embodiments, Pediococcus pentosaceus as provided herein refers to one or more isolated bacterial cells of a bacterial strain having all of the identifying characteristics of the strain deposited with ATCC under accession number 25744; a variant of the strain deposited with ATCC under accession number 25744 having all of the identifying characteristics of the strain ATCC under accession number 25744; and a variant of the strain deposited with ATCC under accession number 25744 having all of the identifying characteristics of the strain ATCC under accession number 25744.

[0133] In embodiments, the composition is effective in increasing anti-inflammatory metabolites. In embodiments, Lactobacillus johnsonii is effective in increasing anti-inflammatory metabolites. In embodiments, Faecalibacterium prausnitzii is effective in increasing anti-inflammatory metabolites. In embodiments, Akkermansia muciniphila is effective in increasing anti-inflammatory metabolites. In embodiments, Myxococcus xanthus is effective in increasing anti-inflammatory metabolites. In embodiments, Pediococcus pentosaceus is effective in increasing anti-inflammatory metabolites. As used herein, "metabolite" refers to intermediates and products of the metabolism of bacterial cells, where the bacterial cells are present in the intestine of a mammal. The term metabolite also includes intermediates and products formed by mammalian cells. Non-limiting examples of metabolites include amino acids, alcohols, vitamins, polyols, organic acids, nucleotides (e.g., inosine-5'-monophosphate and guanosine-5'-monophosphate), lipids, carbohydrates, peptides, and proteins. The term "anti-inflammatory metabolite" as used herein refers to a metabolite produced by a cell (e.g., a bacterial cell, a mammalian cell) that can inhibit inflammation. As defined herein, the terms "inhibition," "inhibit," "inhibiting," and the like, in reference to a protein-anti-inflammatory metabolite interaction, refer to a negative effect (e.g., reduction) on the activity or function of a protein (e.g., reduction of the activity of an inflammatory metabolite) compared to the activity or function of the protein in the absence of an inhibitor (e.g., an anti-inflammatory metabolite). The term "inhibiting" includes, at least in part, partially or completely blocking a stimulus, reducing, preventing, or delaying activation, or inactivating, desensitizing, or downregulating signal transduction, gene expression, enzyme activity, or protein expression (e.g., inflammatory metabolites) required for inflammation.In some embodiments, inhibition refers to the reduction of a disease or a symptom of a disease (e.g., inflammation). Similarly, an "inhibitor" is a compound (e.g., a metabolite) that inhibits inflammation, for example, by binding to an inflammatory metabolite, partially or completely blocking, reducing, preventing, delaying, inactivating, desensitizing, or downregulating the activity of an inflammatory metabolite. As provided herein, a metabolite capable of inhibiting or reducing inflammation refers to a substance that causes a detectably lower activity level of inflammation compared to a control. The reduced activity may be 10%, 20%, 30%, 40%, 50%, 60%, 70%, 80%, 90% or more lower than the activity in the control. In certain examples, the reduction is 1.5-fold, 2-fold, 3-fold, 4-fold, 5-fold, 10-fold, or more than the control.

[0134] In embodiments, the anti-inflammatory metabolite is a microbial lipid or a microbial carbohydrate. In embodiments, the anti-inflammatory metabolite is a microbial lipid. In embodiments, the anti-inflammatory metabolite is a phospholipid. In embodiments, the anti-inflammatory metabolite is a polyunsaturated fatty acid. In embodiments, the anti-inflammatory metabolite is a microbial carbohydrate. In embodiments, the anti-inflammatory metabolite is itaconic acid. In embodiments, the anti-inflammatory metabolite is n-acetylglucosamine. In embodiments, the anti-inflammatory metabolite is n-acetylgalactosamine. In embodiments, the anti-inflammatory metabolite is fucosyllactose. In embodiments, the anti-inflammatory metabolite is an amino acid. In embodiments, the anti-inflammatory metabolite is tryptophan.

[0135] In embodiments, the composition is effective in reducing pro-inflammatory metabolites. In embodiments, the composition is effective in reducing pro-inflammatory metabolites. In embodiments, Lactobacillus johnsonii is effective in reducing pro-inflammatory metabolites. In embodiments, Faecalibacterium prausnitzii is effective in reducing pro-inflammatory metabolites. In embodiments, Akkermansia muciniphila is effective in reducing pro-inflammatory metabolites. In embodiments, Myxococcus xanthus is effective in reducing pro-inflammatory metabolites. In embodiments, Pediococcus pentosaceus is effective in reducing pro-inflammatory metabolites. As provided herein, "pro-inflammatory metabolite" refers to a metabolite produced by a cell (e.g., a bacterial cell, a mammalian cell) that can increase inflammation. As provided herein, a metabolite that can increase inflammation refers to a substance that results in a detectably higher level of inflammation compared to a control. The increased activity may be 10%, 20%, 30%, 40%, 50%, 60%, 70%, 80%, 90% or more greater than the activity in the control. In certain instances, the increase is 1.5-fold, 2-fold, 3-fold, 4-fold, 5-fold, 10-fold or greater compared to the control.

[0136] In embodiments, the pro-inflammatory metabolite is a microbial lipid, a microbial carbohydrate, or a microbial amino acid. In embodiments, the pro-inflammatory metabolite is a microbial lipid. In embodiments, the pro-inflammatory metabolite is dihydroxy-12-octadecenoic acid, cholic acid, or methylmalonic acid. In embodiments, the pro-inflammatory metabolite is a microbial carbohydrate. In embodiments, the pro-inflammatory metabolite is n-acetylmuramic acid, lactobionic acid, or maltotriose. In embodiments, the pro-inflammatory metabolite is a microbial amino acid. In embodiments, the pro-inflammatory metabolite is ornithine or taurine.

[0137] The compositions provided herein may contain metabolically active bacteria or metabolically inactive bacteria or fractions thereof. In some embodiments, Lactobacillus johnsonii, Faecalibacterium prausnitzii, Akkermansia muciniphila, Myxococcus xanthus, and Pediococcus pentosaceus are metabolically active. In some embodiments, Lactobacillus johnsonii, Faecalibacterium prausnitzii, Akkermansia muciniphila, Myxococcus xanthus, and Pediococcus pentosaceus are metabolically inactive. Metabolically active bacteria can divide and produce metabolic products such as carbohydrates, lipids, or amino acids. In contrast, metabolically inactive bacteria do not divide or produce metabolic products. III. Pharmaceutical Compositions

[0138] As described herein, the microbial compositions provided herein can comprise a bacterial population comprising, consisting essentially of, or consisting of any one, two, three, four, five, six, seven, or eight of Lactobacillus sp., Faecalibacterium sp., Akkermansia sp., Myxococcus sp., Cystobacter sp., Pediococcus sp., Bifidobacterium sp., and Clostridium sp. In embodiments, the bacterial population comprises Lactobacillus sp. and Faecalibacterium sp. In some embodiments, the bacterial population includes Lactobacillus sp. and Akkermansia muciniphila. In some embodiments, the bacterial population includes Lactobacillus sp. and Myxococcus xanthus. In some embodiments, the bacterial population includes Lactobacillus sp. and Cystobacter fuscus. In some embodiments, the bacterial population includes Lactobacillus sp. and Pediococcus pentosaceus, Pediococcus acidilactici, Pediococcus damnosus, Pediococcus ethanolidurans, or Pediococcus parvulus. In some embodiments, the bacterial population includes Lactobacillus sp. and Bifidobacterium bifidum, Bifidobacterium pseudolongum, Bifidobacterium saeculare, or Bifidobacterium subtile. In embodiments, the bacterial population comprises Lactobacillus sp. and Clostridium hiranonis. In embodiments, the Lactobacillus sp. is selected from the group consisting of Lactobacillus johnsonii, Lactobacillus rhamnosus, Lactobacillus zeae, Lactobacillus acidipiscis, Lactobacillus acidophilus, Lactobacillus agilis, Lactobacillus aviarius, Lactobacillus brevis, Lactobacillus coleohominis, Lactobacillus crispatus, Lactobacillus crustorum, Lactobacillus curvatus, Lactobacillus diolivorans, Lactobacillus farraginis, Lactobacillus fermentum, and Lactobacillus fuchuensis, Lactobacillus harbinensis, Lactobacillus helveticus, Lactobacillus hilgardii, Lactobacillus intestinalis, Lactobacillus jensenii, Lactobacillus kefiranofaciens, Lactobacillus kefiri, Lactobacillus lindneri, Lactobacillus mali, Lactobacillus manihotivorans, Lactobacillus mucosae, Lactobacillus oeni, Lactobacillus oligofermentans, Lactobacillus panis, Lactobacillus pantheris, Lactobacillus parabrevis, Lactobacillus paracollinoides, Lactobacillus parakefiri, Lactobacillus paraplantarum, Lactobacillus pentosus, Lactobacillus pontis, Lactobacillus reuteri, Lactobacillus rossiae, Lactobacillus salivarius, Lactobacillus siliginis, Lactobacillus sucicola, Lactobacillus vaccinostercus, Lactobacillus vaginalis, Lactobacillus vini, Lactococcus garvieae or Lactococcus lactis. In some embodiments, the Lactobacillus sp. is Lactobacillus johnsonii. In some embodiments, the bacterial population is: Lactobacillus johnsonii, Lactobacillus rhamnosus, Lactobacillus zeae, Lactobacillus acidipiscis, Lactobacillus acidophilus, Lactobacillus agilis, Lactobacillus aviarius, Lactobacillus brevis, Lactobacillus coleohominis, Lactobacillus crispatus, Lactobacillus crustorum, Lactobacillus curvatus, Lactobacillus diolivorans, Lactobacillus farraginis, Lactobacillus fermentum, Lactobacillus fuchuensis, Lactobacillus harbinensis, Lactobacillus helveticus, Lactobacillus hilgardii, Lactobacillus intestinalis, Lactobacillus jensenii, Lactobacillus kefiranofaciens, Lactobacillus kefiri, Lactobacillus lindneri, Lactobacillus mali, Lactobacillus manihotivorans, Lactobacillus mucosae, Lactobacillus oeni, Lactobacillus oligofermentans, Lactobacillus panis, Lactobacillus pantheris, Lactobacillus parabrevis, Lactobacillus paracollinoides, Lactobacillus parakefiri, Lactobacillus paraplantarum, Lactobacillus pentosus, Lactobacillus pontis, Lactobacillus reuteri, Lactobacillus rossiae, Lactobacillussalivarius, Lactobacillus siliginis, Lactobacillus sucicola, Lactobacillus vaccinostercus, Lactobacillus vaginalis, Lactobacillus vini, Lactococcus garvieae, Lactococcus lactis, Faecalibacterium prausnitzii, Akkermansia muciniphila, Myxococcus xanthus, Cystobacter In some embodiments, the bacterial population comprises at least 1, 2, 3, 4, 5, 6, 7, 8, 9, or 10, or 1-5, 1-10, 1-5, or 1-20 of any combination of Lactobacillus fuscus, Pediococcus pentosaceus, Pediococcus acidilactici, Pediococcus damnosus, Pediococcus ethanolidurans, and Pediococcus parvulus. In some embodiments, the bacterial population comprises Lactobacillus johnsonii, Faecalibacterium prausnitzii, Akkermansia muciniphila, Myxococcus xanthus, and / or Pediococcus pentosaceus. In some embodiments, the microbial composition comprises bacterial cells of one or more of the bacterial species Lactobacillus johnsonii, Faecalibacterium prausnitzii, Akkermansia muciniphila, Myxococcus xanthus, or Pediococcus pentosaceus. In embodiments, the composition comprises Lactobacillus johnsonii, Faecalibacterium prausnitzii, Akkermansia muciniphila, Myxococcus xanthus, and Pediococcus pentosaceus. In embodiments, the composition comprises Lactobacillus johnsonii, Faecalibacterium prausnitzii, Akkermansia muciniphila, Myxococcus xanthus, or Pediococcus pentosaceus. In embodiments, the bacterium is an isolated bacterium.

[0139] In embodiments, the microbial composition comprises a therapeutically effective amount of Lactobacillus johnsonii, Faecalibacterium prausnitzii, Akkermansia muciniphila, Myxococcus xanthus, and / or Pediococcus pentosaceus.

[0140] In some embodiments, the microbial composition further comprises a pharmaceutically acceptable excipient. Thus, in one aspect, a pharmaceutical composition is provided comprising a therapeutically effective amount of Lactobacillus johnsonii, Faecalibacterium prausnitzii, Akkermansia muciniphila, Myxococcus xanthus, and Pediococcus pentosaceus, and a pharmaceutically acceptable excipient.

[0141] "Pharmaceutically acceptable excipient" and "pharmaceutically acceptable carrier" refer to substances that aid in the administration and absorption of an active agent by a subject and can be included in the compositions of the present invention without causing significant adverse toxicological effects to the patient. Non-limiting examples of pharmaceutically acceptable excipients include water, NaCl, normal saline solution, lactated Ringer's, normal sucrose, normal glucose, binders, fillers, disintegrants, lubricants, coatings, sweeteners, flavors, salt solutions (e.g., Ringer's solution), alcohols, oils, gelatin, carbohydrates such as lactose, amylose, or starch, fatty acid esters, hydroxymethylcellulose, polyvinylpyrrolidine, and colorants. Such preparations are sterilized and, if desired, can be mixed with auxiliary substances such as lubricants, preservatives, stabilizers, wetting agents, emulsifiers, salts for influencing osmotic pressure, buffers, coloring agents, and / or flavoring agents that do not adversely react with the compounds of the present invention. Those skilled in the art will recognize that other pharmaceutical excipients are useful in the present invention.

[0142] The microbial compositions provided herein, including embodiments thereof, can be administered orally, gastrointestinally, or rectally. Administration can be in the form of a single bolus dose, for example, via a continuous perfusion pump. In some embodiments, the microbial consortium provided herein is combined with one or more excipients, such as disintegrants, fillers, lubricants, or preservatives. In some embodiments, the microbial consortium provided herein forms part of a capsule. Suitable capsules include both hard-shell and soft-shell capsules. Any lipid-based or polymer-based colloid can be used to form the capsule. Exemplary polymers useful for colloid preparation include gelatin, plant polysaccharides or their derivatives, such as carrageenan, and modified forms of starch and cellulose, such as hypromellose. Optionally, other ingredients can be added to the gelling agent solution, such as plasticizers, such as glycerin and / or sorbitol, to reduce capsule hardness, colorants, preservatives, disintegrants, lubricants, and surface treatments.

[0143] The microbial composition can be formulated into a unit dosage form, with each dosage containing, for example, from about 0.005 mg to about 2000 mg of a defined microbial consortium with minimal urease activity per dose. The term "unit dosage form" refers to a physically discrete unit suitable as a unitary dosage for human subjects and other mammals, each unit containing a predetermined quantity of active material, together with appropriate pharmaceutical excipients, calculated to produce the desired therapeutic effect. To prepare solid compositions such as tablets, the primary active ingredient is mixed with a pharmaceutical excipient to form a solid preformulation composition containing a homogeneous mixture of the compounds of the present invention. When these preformulation compositions are referred to as homogeneous, the active ingredient is generally dispersed evenly throughout the composition so that the composition can be easily subdivided into equally effective unit dosage forms such as tablets, pills, and capsules. This solid preformulation is then subdivided into unit dosage forms of the type described above, containing, for example, from 0.005 mg to about 1000 mg of the microbial composition presented herein.

[0144] The microbial compositions can be formulated in unit dosage form, with each dosage being, for example, from about 0.1 mg to about 50 mg, from about 0.1 mg to about 40 mg, from about 0.1 mg to about 20 mg, from about 0.1 mg to about 10 mg, from about 0.2 mg to about 20 mg, from about 0.3 mg to about 15 mg, from about 0.4 mg to about 10 mg, from about 0.5 mg to about 1 mg; from about 0.5 mg to about 100 mg, from about 0.5 mg to about 50 mg, from about 0.5 mg to about 30 mg, from about 0.5 mg to about 20 mg, individually or in combination. g, about 0.5 mg to about 10 mg, about 0.5 mg to about 5 mg; about 1 mg to about 50 mg, about 1 mg to about 30 mg, about 1 mg to about 20 mg, about 1 mg to about 10 mg, about 1 mg to about 5 mg; about 5 mg to about 50 mg, about 5 mg to about 20 mg, about 5 mg to about 10 mg; about 10 mg to about 100 mg, about 20 mg to about 200 mg, about 30 mg to about 150 mg, about 40 mg to about 100 mg, about 50 mg to about 100 mg of Lactobacillus sp. (e.g., Lactobacillus johnsonii), Faecalibacterium sp. (e.g., Faecalibacterium prausnitzii), Akkermansia sp. (e.g., Akkermansia muciniphila), Myxococcus sp. (e.g., Myxococcus xanthus) and / or Pediococcus sp. (e.g., Pediococcus pentosaceus).

[0145] In some embodiments, the tablets or pills of the present invention can be coated or otherwise compounded to provide a dosage form affording the advantage of prolonged action. For example, the tablets or pills can comprise an inner dosage component and an outer dosage component, the latter being in the form of an envelope over the former. The two components can be separated by an enteric layer which serves to resist disintegration in the stomach and permits the inner component to pass intact into the duodenum or to be delayed in release. A variety of materials can be used for such enteric layers or coatings, including several polymeric acids and mixtures of polymeric acids with materials such as shellac, cetyl alcohol, and cellulose acetate.

[0146] Liquid forms into which the compositions of the present invention can be incorporated for oral or injectable administration include aqueous solutions, suitably flavored syrups, aqueous or oily suspensions, and emulsions flavored with edible oils such as cottonseed oil, sesame oil, coconut oil, or peanut oil, as well as elixirs and similar pharmaceutical vehicles. IV. Treatment Methods

[0147] According to the methods provided herein, a subject is administered an effective amount of one or more of the agents provided herein. The terms effective amount and effective dosage are used interchangeably. The term effective amount is defined as any amount necessary to produce a desired physiological response (e.g., reduction of inflammation, infection, or dysbiosis). Effective amounts and schedules for administering agents can be empirically determined by those of skill in the art. The dosage range for administration is large enough to produce the desired effect of affecting (e.g., reducing or delaying) one or more symptoms of a disease or disorder. The dosage should not be so large as to cause substantial adverse side effects, such as undesirable cross-reactions, anaphylactic reactions, etc. Generally, dosages vary depending on age, condition, sex, type of disease, severity of disease or disorder, route of administration, or whether other drugs are included in the regimen, and can be determined by one of skill in the art. Dosages can be adjusted by the individual physician in the event of any contraindications. Dosages can vary and can be administered daily, daily, or over several days, in one or more doses. Guidance can be found in the literature regarding appropriate dosages for a given class of pharmaceutical product. For example, with respect to a given parameter, an effective amount indicates an increase or decrease of at least 5%, 10%, 15%, 20%, 25%, 40%, 50%, 60%, 75%, 80%, 90%, or at least 100%. Efficacy can also be expressed as a "-fold" increase or decrease. For example, a therapeutically effective amount may have an effect that is at least 1.2-fold, 1.5-fold, 2-fold, 5-fold, or greater than the control. The exact dosage and formulation will depend on the purpose of the treatment and can be ascertained by one of ordinary skill in the art using known techniques (see, e.g., Lieberman, Pharmaceutical Dosage Forms (Vols. 1-3, 1992); Lloyd, The See Art, Science and Technology of Pharmaceutical Compounding (1999); Remington: The Science and Practice of Pharmacy, 20th Edition, Gennaro, Editor (2003) and Pickar, Dosage Calculations (1999).

[0148] For prophylactic use, a therapeutically effective amount of a microbial composition described herein is administered to a subject prior to or during initial onset (e.g., at the first signs and symptoms of an autoimmune disease). Therapeutic treatment involves administering a therapeutically effective amount of an agent described herein to a subject after diagnosis or onset of disease. Thus, in another aspect, methods are provided for treating a disease (e.g., an inflammatory disease, an infection, or a dysbiosis) in a subject in need thereof.

[0149] The terms "subject," "patient," "individual," and the like are not limiting and are generally interchangeable, i.e., an individual described as a "patient" does not necessarily have a given disease, but may simply be seeking medical advice.

[0150] As used herein, "treating" or "treatment" of a condition, disease, or disorder, or symptoms associated with a condition, disease, or disorder, refers to an approach for obtaining beneficial or desired results, including clinical results. Beneficial or desired clinical results can include, but are not limited to, alleviation or amelioration of one or more symptoms or conditions, reduction in the severity of a condition, disorder, or disease, stabilization of a condition, disorder, or disease state, prevention of the onset of a condition, disorder, or disease, prevention of the spread of a condition, disorder, or disease, delaying or slowing the progression of a condition, disorder, or disease, delaying or slowing the onset of a condition, disorder, or disease, improvement or palliation of a condition, disorder, or disease state, and remission, whether partial or complete. "Treating" can also mean extending the survival of a subject beyond that expected in the absence of treatment. "Treating" can mean inhibiting the progression of a condition, disorder, or disease, or temporarily slowing the progression of a condition, disorder, or disease, although in some instances, it involves permanently halting the progression of a condition, disorder, or disease. As used herein, the terms treatment, treat, or treating refer to a method of reducing the effects of one or more symptoms of a disease or condition characterized by the expression of a protease, or the symptoms of a disease or condition characterized by the expression of a protease. Thus, in the disclosed methods, treatment can refer to a 10%, 20%, 30%, 40%, 50%, 60%, 70%, 80%, 90%, or 100% reduction in the severity of an established disease, condition, or symptom of a disease or condition (e.g., inflammation, infection, or dysbiosis). For example, a method for treating a disease is considered treatment if one or more symptoms of the disease are reduced by 10% in a subject compared to a control. Thus, the reduction can be a 10%, 20%, 30%, 40%, 50%, 60%, 70%, 80%, 90%, 100%, or any percentage reduction between 10% and 100% compared to native or control levels.It is understood that treatment does not necessarily refer to a cure or complete elimination of a disease, condition, or symptoms of a disease or condition. Furthermore, as used herein, reference to decrease, reduction, or inhibition includes a 10%, 20%, 30%, 40%, 50%, 60%, 70%, 80%, 90% or greater change compared to control levels, and such terms can, but do not necessarily, include complete elimination.

[0151] The composition containing the defined microbial composition can be administered to the subject's gastrointestinal tract via a nasoduodenal catheter, via an enema, via an endoscope, enteroscope, or colonoscope, or orally as a capsule or pill that can be consumed. In certain embodiments, the defined microbial composition is diluted in an appropriate excipient (e.g., saline solution). In a preferred embodiment, the bacteria is delivered in a lyophilized form.

[0152] Regardless of how the composition is formulated, the required dosage will depend on the route of administration, the nature of the formulation, the nature of the subject's condition (e.g., immune system immaturity or gastrointestinal disorders), the subject's size, weight, body surface area, age, and sex, other medications being administered, and the judgment of the attending clinician. In some embodiments, a suitable dosage ranges from 0.01 to 1,000 mg / kg. Some typical dosage ranges are from about 1 μg / kg to about 1 g / kg of body weight per day. In some embodiments, the dosage range is from about 0.01 mg / kg to about 100 mg / kg of body weight per day. In some embodiments, the dosage may be, for example, 1 mg / kg, 2 mg / kg, 5 mg / kg, 10 mg / kg, 20 mg / kg, 50 mg / kg, or 100 mg / kg. Alternatively, or in addition, dosage may be expressed as cfu or cfu / g dry weight. In some embodiments, dosage may vary, but is typically about 10 2 ~about 10 12 cfu / g, e.g., 1xl0 2 cfu / g, 5xl0 2 cfu / g, 1xl0 3 cfu / g, 5xl0 3 cfu / g, 1xl04 cfu / g, 5xl0 4 cfu / g, 1xl0 5 cfu / g, 5xl0 5 cfu / g, 1xl0 6 cfu / g, 5xl0 6 cfu / g, 1xl0 7 cfu / g, 5xl0 7 cfu / g, 1xl0 8 cfu / g, 5xl0 8 cfu / g, 1xl0 9 cfu / g, 5xl0 9 cfu / g, 1xl0 10 cfu / g, 5xl0 10 cfu / g, lxl0 11 cfu / g, 5xl0 11 cfu / g or 1xl0 12 The dose can range from about 10 cfu / g dry weight of the administered bacteria (individually) or the equivalent of the total population of bacteria. 2 ~about 10 12 cfu, e.g., 1x10 2 cfu, 5xl0 2 cfu, 1xl0 3 cfu, 5xl0 3 cfu, 1xl0 4 cfu, 5xl0 4 cfu, 1xl0 5 cfu, 5xl0 5 cfu, 1xl0 6 cfu, 5xl0 6 cfu, 1xl0 7 cfu, 5xl0 7 cfu, 1xl0 8 cfu, 5xl0 8 cfu, 1xl0 9 cfu, 5xl0 9 cfu, 1xl0 10 cfu, 5xl0 10 cfu, lxl0 11 cfu, 5xl0 11 cfu or 1xl0 12 The cfu administered can range from any one of the bacteria (individually) or the total population of bacteria.

[0153] Administration can be single or multiple (e.g., 2x, 3x, 4x, 6x, 8x, 10x, 20x, 50x, 100x, 150x, or more multiples). The duration of treatment with any of the compositions provided herein can be any length of time, from as short as one day to as long as the lifespan of the host (e.g., many years). For example, the composition can be administered 1, 2, 3, 4, 5, 6, or 7 times per week (e.g., for 4 weeks to several months or years); once per month (e.g., for 3 to 12 months or years); or once per year, for 5, 10 years, or longer. It is also worth noting that the frequency of treatment can vary. For example, the composition can be administered daily, weekly, monthly, or once (or twice, three times, etc.) per year.

[0154] The composition can also be administered in conjunction with other therapeutic agents. The other therapeutic agents vary depending on the specific disorder, but can include, for example, dietary modification, hemodialysis, sodium benzoate, phenylacetate, arginine, or surgical therapy. Concurrent administration of two or more therapeutic agents does not require the agents to be administered at the same time or by the same route, as long as the period during which the agents exert their therapeutic effects overlaps. Simultaneous or sequential administration is contemplated, as is administration on different days or weeks.

[0155] Presented herein are methods for treating and preventing inflammatory diseases, infectious diseases (e.g., respiratory or gastrointestinal infections), and dysbiosis, comprising administering a bacterial population or microbial composition described herein, including embodiments thereof.

[0156] In certain aspects, methods are provided for treating or preventing a dysbiosis, an inflammatory disease, or a viral respiratory infection in a subject in need thereof.

[0157] In certain embodiments, methods are provided for increasing the level of an anti-inflammatory compound and / or decreasing the level of a pro-inflammatory compound in a subject in need thereof.

[0158] In one aspect, a method of altering the metabolism of a subject in need thereof is provided.

[0159] In embodiments, the method includes administering to the subject an effective amount of a bacterial population comprising, consisting essentially of, or consisting of 1, 2, 3, 4, 5, 6, 7, or 8 (or at least 1, 2, 3, 4, 5, 6, 7, or 8) bacterial species. In embodiments, the bacterial population comprises, consists essentially of, or consists of any one, two, three, four, five, six, seven, or eight of Lactobacillus sp., Faecalibacterium sp., Akkermansia sp., Myxococcus sp., Cystobacter sp., Pediococcus sp., Bifidobacterium sp., and Clostridium sp. In embodiments, the bacterial population includes Lactobacillus sp. and Faecalibacterium prausnitzii. In embodiments, the bacterial population includes Lactobacillus sp. and Akkermansia muciniphila. In some embodiments, the bacterial population includes a Lactobacillus sp. and Myxococcus xanthus. In some embodiments, the bacterial population includes a Lactobacillus sp. and Cystobacter fuscus. In some embodiments, the bacterial population includes a Lactobacillus sp. and Pediococcus pentosaceus, Pediococcus acidilactici, Pediococcus damnosus, Pediococcus ethanolidurans, or Pediococcus parvulus. In some embodiments, the bacterial population includes a Lactobacillus sp. and Bifidobacterium bifidum, Bifidobacterium pseudolongum, Bifidobacterium saeculare, or Bifidobacterium subtile. In some embodiments, the bacterial population includes a Lactobacillus sp. and Clostridium hiranonis.In some embodiments, Lactobacillus sp. is Lactobacillus johnsonii, Lactobacillus rhamnosus, Lactobacillus zeae, Lactobacillus acidipiscis, Lactobacillus acidophilus, Lactobacillus agilis, Lactobacillus aviarius, Lactobacillus brevis, Lactobacillus coleohominis, Lactobacillus crispatus, Lactobacillus crustorum, Lactobacillus curvatus, Lactobacillus diolivorans, Lactobacillus farraginis, Lactobacillus fermentum, Lactobacillus fuchuensis, Lactobacillus harbinensis, Lactobacillus helveticus, Lactobacillus hilgardii, Lactobacillus intestinalis, Lactobacillus jensenii, Lactobacillus kefiranofaciens, Lactobacillus kefiri, Lactobacillus lindneri, Lactobacillus mali, Lactobacillus manihotivorans, Lactobacillus mucosae, Lactobacillus oeni, Lactobacillus. oligofermentans、Lactobacillus panis、Lactobacillus pantheris、Lactobacillus parabrevis、Lactobacillus paracollinoides、Lactobacillus parakefiri、Lactobacillus paraplantarum、Lactobacillus pentosus、Lactobacillus pontheris reuteri、Lactobacillus rossiae、Lactobacillus salivarius、Lactobacillus siliginis、Lactobacillus sucicola、Lactobacillus vaccinostercus、Lactobacillus vaginalis、Lactobacillus vini、Lactococcus garviee、LactobacillusはLacoccus lactis, Lactobacillus sp., Lactobacillus johnsonii, Lactobacillus rhamnosus, Lactobacillus johnsonii, Lactobacillus rhamnosuscillus, Lactobacillus zea acidipiscis, Lactobacillus acidophilus, Lactobacillus agilis, Lactobacillus aviarius, Lactobacillus brevis, Lactobacillus coleohominis, Lactobacillus crispatus, Lactobacillus crustorum, Lactobacillus curvatus, Lactobacillus diolivorans, Lactobacillus farraginis, Lactobacillus fermentum, Lactobacillus fuchuensis, Lactobacillus harbinensis, Lactobacillus helveticus, Lactobacillus hilgardii, Lactobacillus intestinalis, Lactobacillus jensenii, Lactobacillus kefiranofaciens、Lactobacillus kefiri、Lactobacillus lindneri、Lactobacillus mali、Lactobacillus manihotivorans、Lactobacillus mucosae、Lactobacillus oeni、Lactobacillus oligofermentans、Lactobacillus pactobacillus、Lactobacillus pactobacillus pantheris、Lactobacillus parabrevis、Lactobacillus paracollinoides、Lactobacillus parakefiri、Lactobacillus paraplantarum、Lactobacillus pentosus、Lactobacillus pontis、Lactobacillus reuterilus、Lactobacillus rossiaellus、Lactobacillus salivarius、Lactobacillus siliginis、Lactobacillus sucicola、Lactobacillus vaccinostercus、Lactobacillus vaginalis、Lactobacillus vini、Lactococcus garvieae、Lactococcus lactis、Faecalibacterium pratzinikkersia muciniphila、Myxococcus xanthus、Cystobacter fuscus、Pediococcus pentosaceus、Pediococcus acidilactici、Pediococcus damnosus、Pediococcus ethanolidurans、Pediococcus parvulus 1, 2, 3, 4, 5, 6, 7, 8, 9, 5, 6, 7, 8, 9, 10 1~5ぁ1~10め1~5または1~20 Lactobacillus johnsonii、Faecalibacterium prausnitzii、Akkermansia muciniphila, Myxococcus xanthus, and / or Pediococcus pentosaceus. In embodiments, the bacterium is an isolated bacterium.

[0160] In embodiments, the method further comprises the step of: and / or Pediococcus sp. to the subject. In some embodiments, (i) the Lactobacillus sp. is Lactobacillus johnsonii, (ii) the Faecalibacterium sp. is Faecalibacterium prausnitzii, and (iii) the Akkermansia sp. is Akkermansia muciniphila, (iv) Myxococcus sp. is Myxococcus xanthus, and (v) Pediococcus sp. is Pediococcus pentosaceus. In some embodiments, (i) Lactobacillus sp. is Lactobacillus zeae, Lactobacillus acidipiscis, Lactobacillus acidophilus, Lactobacillus agilis, Lactobacillus aviarius, Lactobacillus brevis, Lactobacillus coleohominis, Lactobacillus crispatus, Lactobacillus crustorum, Lactobacillus curvatus, Lactobacillus diolivorans, Lactobacillus farraginis, Lactobacillus fermentum, Lactobacillus fuchuensis, Lactobacillus harbinensis, Lactobacillus helveticus, Lactobacillus hilgardii, Lactobacillus intestinalis, Lactobacillus jensenii, Lactobacillus kefiranofaciens, Lactobacillus kefiri, Lactobacillus lindneri, Lactobacillus mali, Lactobacillus manihotivorans, Lactobacillus mucosae, Lactobacillus oeni, Lactobacillus oligofermentans, Lactobacillus panis, Lactobacillus pantheris, Lactobacillus parabrevis, Lactobacillus paracollinoides, Lactobacillus parakefiri, Lactobacillus paraplantarum, Lactobacillus pentosus, Lactobacillus pontis, Lactobacillus reuteri, Lactobacillus rossiae, Lactobacillus salivarius, Lactobacillus siliginis, Lactobacillus sucicola, Lactobacillus vaccinostercus, Lactobacillus vaginalis, Lactobacillus vini, Lactococcus garvieae or Lactococcus lactis; (ii) Faecalibacterium sp. is Faecalibacterium prausnitzii; (iii) Akkermansia sp. is Akkermansia muciniphila; (iv) Myxococcus sp. is Myxococcus xanthus; (v) Pediococcus sp. is Pediococcus pentosaceus, Pediococcus acidilactici, Pediococcus damnosus, Pediococcus ethanolidurans or Pediococcus It's a little one.

[0161] In embodiments, the Myxococcus sp. is in the form of spores, vegetative bacteria, or a mixture of spores and vegetative bacteria. In embodiments, the Myxococcus sp. is in the form of a powder containing spores. In embodiments, the Clostridium sp. is in the form of spores, vegetative bacteria, or a mixture of spores and vegetative bacteria. In embodiments, the Clostridium sp. is in the form of a powder containing spores.

[0162] In embodiments, fewer than about 20, 15, 10, 9, 8, 7, or 6 different species of bacteria are administered to the subject. In embodiments, fewer than about 20 different species of bacteria are administered to the subject. In embodiments, fewer than 20 different species of bacteria are administered to the subject. In embodiments, fewer than about 15 different species of bacteria are administered to the subject. In embodiments, fewer than 15 different species of bacteria are administered to the subject. In embodiments, fewer than 10 different species of bacteria are administered to the subject. In embodiments, fewer than 10 different species of bacteria are administered to the subject. In embodiments, fewer than about 9 different species of bacteria are administered to the subject. In embodiments, fewer than 9 different species of bacteria are administered to the subject. In embodiments, fewer than about 8 different species of bacteria are administered to the subject. In embodiments, fewer than 8 different species of bacteria are administered to the subject. In embodiments, fewer than about 7 different species of bacteria are administered to the subject. In some embodiments, fewer than seven different species of bacteria are administered to the subject. In some embodiments, fewer than about six different species of bacteria are administered to the subject. In some embodiments, fewer than six different species of bacteria are administered to the subject.

[0163] In embodiments, the bacterial population forms part of a bacterial composition. In embodiments, the bacterial composition comprises less than about 20, 15, 10, 9, 8, 7, or 6 species of bacteria. In embodiments, the bacterial composition comprises less than about 20 species of bacteria. In embodiments, the bacterial composition comprises less than 20 species of bacteria. In embodiments, the bacterial composition comprises less than 20 species of bacteria. In embodiments, the bacterial composition comprises less than about 15 species of bacteria. In embodiments, the bacterial composition comprises less than 15 species of bacteria. In embodiments, the bacterial composition comprises less than 15 species of bacteria. In embodiments, the bacterial composition comprises less than 10 species of bacteria. In embodiments, the bacterial composition comprises less than 10 species of bacteria. In embodiments, the bacterial composition comprises less than 9 species of bacteria. In embodiments, the bacterial composition comprises less than 9 species of bacteria. In embodiments, the bacterial composition comprises less than 8 species of bacteria. In embodiments, the bacterial composition comprises less than 8 species of bacteria. In embodiments, the bacterial composition comprises less than 7 species of bacteria. In embodiments, the bacterial composition comprises less than 7 species of bacteria. In embodiments, the bacterial composition comprises less than 6 species of bacteria. In embodiments, the bacterial composition comprises fewer than six species of bacteria.

[0164] In some embodiments, the bacterial composition further comprises a pharmaceutically acceptable excipient. In some embodiments, the bacterial composition is not a fecal transplant. In some embodiments, the bacterial composition is a capsule, tablet, suspension, suppository, powder, cream, oil, oil-in-water emulsion, water-in-oil emulsion, or aqueous solution. In some embodiments, the bacterial composition is in the form of a powder, solid, semi-solid, or liquid.

[0165] In embodiments, the bacterial composition has a water activity (a) of less than about 0.9, 0.8, 0.7, 0.6, 0.5, 0.4, 0.3, 0.2, or 0.1 at 20°C. w In some embodiments, the bacterial composition has an a of less than about 0.9 at 20°C. w In embodiments, the bacterial composition has an a of less than 0.9 at 20°C. wIn embodiments, the bacterial composition has an a of less than about 0.8 at 20°C. w In some embodiments, the bacterial composition has an a of less than 0.8 at 20°C. w In embodiments, the bacterial composition has an a of less than about 0.7 at 20°C. w In embodiments, the bacterial composition has an a of less than 0.7 at 20°C. w In embodiments, the bacterial composition has an a of less than about 0.6 at 20°C. w In some embodiments, the bacterial composition has an a of less than 0.6 at 20°C. w In embodiments, the bacterial composition has an a of less than about 0.5 at 20°C. w In embodiments, the bacterial composition has an a of less than 0.5 at 20°C. w In embodiments, the bacterial composition has an a of less than about 0.4 at 20°C. w In some embodiments, the bacterial composition has an a of less than 0.4 at 20°C. w In embodiments, the bacterial composition has an a of less than about 0.3 at 20°C. w In some embodiments, the bacterial composition has an a of less than 0.3 at 20°C. w In embodiments, the bacterial composition has an a of less than about 0.2 at 20°C. w In embodiments, the bacterial composition has an a of less than 0.2 at 20°C. w In embodiments, the bacterial composition has an a of less than about 0.1 at 20°C. w In some embodiments, the bacterial composition has an a of less than 0.1 at 20°C. w It has.

[0166] In embodiments, the bacterial composition is a food or beverage.

[0167] In embodiments, the bacterial composition is administered orally or rectally.

[0168] In embodiments, the Lactobacillus sp., Faecalibacterium sp., Akkermansia sp., Myxococcus sp., and / or Pediococcus sp. are in powder form. In embodiments, the Lactobacillus sp., Faecalibacterium sp., Akkermansia sp., Myxococcus sp., and / or Pediococcus sp. are lyophilized.

[0169] In embodiments, the subject is a human, hi embodiments, the subject has or lives with someone who has a bacterial, viral, or fungal gastrointestinal infection.

[0170] In embodiments, the subject has an inflammatory disease. In embodiments, the subject is at risk of developing an inflammatory disease. In embodiments, the subject has at least one, two, three, or four cousins, grandparents, parents, aunts, uncles, and / or siblings who have been diagnosed with an inflammatory disease. In embodiments, the subject has at least four cousins, grandparents, parents, aunts, uncles, and / or siblings who have been diagnosed with an inflammatory disease. In embodiments, the subject has at least three cousins, grandparents, parents, aunts, uncles, and / or siblings who have been diagnosed with an inflammatory disease. In embodiments, the subject has at least two cousins, grandparents, parents, aunts, uncles, and / or siblings who have been diagnosed with an inflammatory disease. In embodiments, the subject has at least one cousin, grandparent, parent, aunts, uncles, and / or siblings who has been diagnosed with an inflammatory disease.

[0171] In embodiments, the inflammatory disease is selected from the group consisting of allergies, atopy, asthma, autoimmune diseases, autoinflammatory diseases, hypersensitivity, childhood allergic asthma, allergic asthma, inflammatory bowel disease, celiac disease, Crohn's disease, colitis, ulcerative colitis, collagenous colitis, lymphocytic colitis, diverticulitis, irritable bowel syndrome, short bowel syndrome, blind loop syndrome, chronic persistent diarrhea, refractory diarrhea of ​​infancy, traveler's diarrhea, immunoproliferative small bowel disease, chronic prostatitis, post-enteritis syndrome, tropical sprue, Whipple's disease, Wolman's disease, arthritis, rheumatoid arthritis, Behcet's disease, uveitis, pyoderma gangrenosum, and ulcerative colitis. These include erythema nodosum, traumatic brain injury, psoriatic arthritis, juvenile idiopathic arthritis, multiple sclerosis, systemic lupus erythematosus (SLE), myasthenia gravis, juvenile-onset diabetes, type 1 diabetes, Guillain-Barré syndrome, Hashimoto's encephalitis, Hashimoto's thyroiditis, ankylosing spondylitis, psoriasis, Sjögren's syndrome, vasculitis, glomerulonephritis, autoimmune thyroiditis, bullous pemphigoid, sarcoidosis, ichthyosis, Graves' ophthalmopathy, Addison's disease, vitiligo, acne vulgaris, pelvic inflammatory disease, reperfusion injury, sarcoidosis, graft rejection, interstitial cystitis, atherosclerosis, and atopic dermatitis.

[0172] In embodiments, the inflammatory disease is pediatric allergic asthma or inflammatory bowel disease. In embodiments, the subject suffers from constipation, diarrhea, bloating, urinary urgency, and / or abdominal pain.

[0173] In embodiments, the subject has received an antibiotic within the last 1, 2, 3, or 4 months. In embodiments, the subject has received an antibiotic within the last 4 months. In embodiments, the subject has received an antibiotic within the last 3 months. In embodiments, the subject has received an antibiotic within the last 2 months. In embodiments, the subject has received an antibiotic within the last month.

[0174] In embodiments, the subject is a newborn. In embodiments, the subject is less than about 1, 2, 3, 4, 5, 6, 7, 8, 9, 12, 18, or 24 months old. In embodiments, the subject is less than about 1 month old. In embodiments, the subject is less than 1 month old. In embodiments, the subject is less than about 2 months old. In embodiments, the subject is less than 2 months old. In embodiments, the subject is less than about 3 months old. In embodiments, the subject is less than 3 months old. In embodiments, the subject is less than about 4 months old. In embodiments, the subject is less than 4 months old. In embodiments, the subject is less than about 5 months old. In embodiments, the subject is less than 5 months old. In embodiments, the subject is less than about 6 months old. In embodiments, the subject is less than 6 months old. In embodiments, the subject is less than about 7 months old. In embodiments, the subject is less than 7 months old. In embodiments, the subject is less than about 8 months old. In embodiments, the subject is less than 8 months old. In embodiments, the subject is less than about 9 months old. In embodiments, the subject is less than 9 months old. In embodiments, the subject is less than about 12 months old. In embodiments, the subject is less than 12 months old. In embodiments, the subject is less than about 18 months old. In embodiments, the subject is less than 18 months old. In embodiments, the subject is less than about 24 months old. In embodiments, the subject is less than 24 months old.

[0175] In embodiments, the subject is between about 2 and about 18 years old, or at least about 18 years old. In embodiments, the subject is between about 2 and about 18 years old, or at least 18 years old. In embodiments, the subject is between about 2 and about 18 years old, or at least about 18 years old (e.g., 19, 20, 25, 30, 40, 50, 60, 70, 80, 90) years old. In embodiments, the subject is between about 2 and about 18 years old, or about 19 years old. In embodiments, the subject is between about 2 and about 18 years old, or about 19 years old. In embodiments, the subject is between about 2 and about 18 years old, or about 20 years old. In embodiments, the subject is between about 2 and about 18 years old, or about 20 years old. In embodiments, the subject is between about 2 and about 18 years old, or about 25 years old. In embodiments, the subject is between about 2 and about 18 years old, or about 25 years old. In embodiments, the subject is between about 2 and about 18 years old, or about 30 years old. In embodiments, the subject is between about 2 and about 18 years old, or about 30 years old. In embodiments, the subject is between about 2 and about 18 years old, or about 40 years old. In embodiments, the subject is between about 2 and about 18 years old, or about 40 years old. In embodiments, the subject is between about 2 and about 18 years old, or about 50 years old. In embodiments, the subject is between about 2 and about 18 years old, or about 50 years old. In embodiments, the subject is between about 2 and about 18 years old, or about 60 years old. In embodiments, the subject is between about 2 and about 18 years old, or about 60 years old. In embodiments, the subject is between about 2 and about 18 years old, or about 70 years old. In embodiments, the subject is between about 2 and about 18 years old, or is 70 years old. In embodiments, the subject is between about 2 and about 18 years old, or is about 80 years old. In embodiments, the subject is between about 2 and about 18 years old, or is 80 years old. In embodiments, the subject is between about 2 and about 18 years old, or is about 90 years old. In embodiments, the subject is between about 2 and about 18 years old, or is 90 years old.

[0176] In embodiments, the subject has (a) an increased rate of Streptococcus spp., Bifidobacterium spp., and Enterococcus spp. compared to a healthy or general population; (b) a decreased rate of Alternaria alternata, Aspergillus flavus, Aspergillus cibarius, and Candida sojae compared to a healthy or general population; (c) an increased rate of Candida albicans and Debaryomyces spp. compared to a healthy or general population; (d) a decreased rate of Bifidobacteria spp., Lactobacillus spp., Faecalibacterium spp., and Akkermansia spp. compared to a healthy or general population; (e) a decreased rate of Malassezia spp. compared to a healthy or general population; or (f) a decreased rate of Bacterioides spp., Ruminococcus spp., Prevotella spp. compared to a healthy or general population. or (g) a gastrointestinal microbiome that has an increased proportion of Enterococcus faecalis, Enterococcus faecium, or Clostridium difficile compared to a healthy or general population.

[0177] In embodiments, the effective amount is (i) a Bifidobacterium sp., Clostridia sp. belonging to clade IV or XIV, Lachnospira sp., and / or Ruminococcus in the subject. sp. level; (ii) decreasing the pH in the subject's feces; (iii) increasing the level of lactic acid in the subject's feces; (iv) increasing the level of circulating itaconate in the subject; (v) treating, reducing, or preventing allergic inflammation in the subject; (vi) decreasing the adaptive immune response in the subject's airway; (vii) decreasing dendritic cell activation in the gastrointestinal-associated mesenteric lymph nodes; (viii) increasing the level of reparative macrophages in the subject's lungs, blood, serum, or plasma; (ix) increasing the level of an anti-inflammatory compound in the subject; (x) decreasing the level of a pro-inflammatory compound in the subject; (xi) decreasing the level of eotaxin expression and / or secretion in the subject; and / or (xii) decreasing the level of mucin expression and / or secretion in the subject.

[0178] In embodiments, the effective amount is effective to reduce secretion and / or levels of secretion of mucin in the lungs of said subject.

[0179] In embodiments, the anti-inflammatory compound is a cytokine, a microbial lipid, a microbial carbohydrate, or a microbial amino acid. In embodiments, the anti-inflammatory compound is IL-17. In embodiments,

[0180] In embodiments, the pro-inflammatory compound is a cytokine, a microbial lipid, a microbial carbohydrate, or a microbial amino acid. In embodiments, the pro-inflammatory compound is IL-4, IL-10, IL-8, IL-13, TNF-α, or MUC5B.

[0181] In embodiments, the Lactobacillus sp., Faecalibacterium sp., Akkermansia sp., Myxococcus sp., and / or Pediococcus sp. are metabolically active. In embodiments, the Lactobacillus sp., Faecalibacterium sp., Akkermansia sp., Myxococcus sp., and / or Pediococcus sp. are metabolically inactive.

[0182] In several embodiments, the method further comprises administering to the subject (a) a Bifidobacterium sp., (b) a Cystobacter sp., or (c) a fungal microorganism.

[0183] In some embodiments, the effective amount is effective to alter the metabolism of the subject. In some embodiments, altering the metabolism of the subject comprises increasing the level of a lipid, phospholipid, or plasmalogen. In some embodiments, altering the metabolism of the subject comprises increasing the level of any compound listed in Table 3, or any combination of at least 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 16, 17, 18, 19, 20, 21, 22, 23, 24, or 25 compounds listed in Table 3 in the subject. In some embodiments, altering the metabolism of the subject comprises increasing the level of any compound listed in Table 3, or any combination of two compounds listed in Table 3 in the subject. In embodiments, altering the metabolism of a subject comprises increasing the level of any compound listed in Table 3, or any combination of three compounds listed in Table 3, in the subject. In embodiments, altering the metabolism of a subject comprises increasing the level of any compound listed in Table 3, or any combination of four compounds listed in Table 3, in the subject. In embodiments, altering the metabolism of a subject comprises increasing the level of any compound listed in Table 3, or any combination of five compounds listed in Table 3, in the subject. In embodiments, altering the metabolism of a subject comprises increasing the level of any compound listed in Table 3, or any combination of six compounds listed in Table 3, in the subject. In embodiments, altering the metabolism of a subject comprises increasing the level of any compound listed in Table 3, or any combination of seven compounds listed in Table 3, in the subject. In embodiments, altering the metabolism of a subject comprises increasing the level of any compound listed in Table 3, or any combination of the eight compounds listed in Table 3, in the subject.In embodiments, altering the metabolism of a subject comprises increasing the level of any compound listed in Table 3, or any combination of the nine compounds listed in Table 3, in the subject. In embodiments, altering the metabolism of a subject comprises increasing the level of any compound listed in Table 3, or any combination of the ten compounds listed in Table 3, in the subject. In embodiments, altering the metabolism of a subject comprises increasing the level of any compound listed in Table 3, or any combination of the eleven compounds listed in Table 3, in the subject. In embodiments, altering the metabolism of a subject comprises increasing the level of any compound listed in Table 3, or any combination of the twelve compounds listed in Table 3, in the subject. In embodiments, altering the metabolism of a subject comprises increasing the level of any compound listed in Table 3, or any combination of the thirteen compounds listed in Table 3, in the subject. In embodiments, altering the metabolism of a subject comprises increasing the level of any compound listed in Table 3 or any combination of the 14 compounds listed in Table 3 in the subject. In embodiments, altering the metabolism of a subject comprises increasing the level of any compound listed in Table 3 or any combination of the 15 compounds listed in Table 3 in the subject. In embodiments, altering the metabolism of a subject comprises increasing the level of any compound listed in Table 3 or any combination of the 16 compounds listed in Table 3 in the subject. In embodiments, altering the metabolism of a subject comprises increasing the level of any compound listed in Table 3 or any combination of the 17 compounds listed in Table 3 in the subject. In embodiments, altering the metabolism of a subject comprises increasing the level of any compound listed in Table 3 or any combination of the 18 compounds listed in Table 3 in the subject.In embodiments, altering the metabolism of a subject comprises increasing the level of any compound listed in Table 3 or any combination of the 19 compounds listed in Table 3 in the subject. In embodiments, altering the metabolism of a subject comprises increasing the level of any compound listed in Table 3 or any combination of the 20 compounds listed in Table 3 in the subject. In embodiments, altering the metabolism of a subject comprises increasing the level of any compound listed in Table 3 or any combination of the 21 compounds listed in Table 3 in the subject. In embodiments, altering the metabolism of a subject comprises increasing the level of any compound listed in Table 3 or any combination of the 22 compounds listed in Table 3 in the subject. In embodiments, altering the metabolism of a subject comprises increasing the level of any compound listed in Table 3 or any combination of the 23 compounds listed in Table 3 in the subject. In embodiments, altering the metabolism of the subject comprises increasing the level of any compound listed in Table 3, or any combination of the 24 compounds listed in Table 3, in the subject. In embodiments, altering the metabolism of the subject comprises increasing the level of any compound listed in Table 3, or any combination of the 25 compounds listed in Table 3, in the subject. In embodiments, the level is increased in the subject's feces. In embodiments, the level is increased in the subject's body fluids. In embodiments, altering the metabolism of the subject comprises decreasing the level of carbohydrates, lipids, or energy compounds in the subject. In embodiments, altering the metabolism of a subject comprises decreasing the level of any compound listed in Table 4, or any combination of at least 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 16, 17, 18, 19, 20, 21, 22, 23, 24, 25, 30, 35, 40, 45, or 50 compounds listed in Table 4 in the subject.In embodiments, altering the metabolism of a subject comprises decreasing the level of any compound listed in Table 4, or any combination of two compounds listed in Table 4, in the subject. In embodiments, altering the metabolism of a subject comprises decreasing the level of any compound listed in Table 4, or any combination of three compounds listed in Table 4, in the subject. In embodiments, altering the metabolism of a subject comprises decreasing the level of any compound listed in Table 4, or any combination of four compounds listed in Table 4, in the subject. In embodiments, altering the metabolism of a subject comprises decreasing the level of any compound listed in Table 4, or any combination of five compounds listed in Table 4, in the subject. In embodiments, altering the metabolism of a subject comprises decreasing the level of any compound listed in Table 4, or any combination of six compounds listed in Table 4, in the subject. In embodiments, altering the metabolism of a subject comprises decreasing the level of any compound listed in Table 4, or any combination of seven compounds listed in Table 4, in the subject. In embodiments, altering the metabolism of the subject comprises decreasing the level in the subject of any compound listed in Table 4, or any combination of the eight compounds listed in Table 4. In embodiments, altering the metabolism of the subject comprises decreasing the level in the subject of any compound listed in Table 4, or any combination of the nine compounds listed in Table 4. In embodiments, altering the metabolism of the subject comprises decreasing the level in the subject of any compound listed in Table 4, or any combination of the ten compounds listed in Table 4. In embodiments, altering the metabolism of the subject comprises decreasing the level in the subject of any compound listed in Table 4, or any combination of the eleven compounds listed in Table 4.In embodiments, altering the metabolism of a subject comprises decreasing the level of any compound listed in Table 4 or any combination of the 12 compounds listed in Table 4 in the subject. In embodiments, altering the metabolism of a subject comprises decreasing the level of any compound listed in Table 4 or any combination of the 13 compounds listed in Table 4 in the subject. In embodiments, altering the metabolism of a subject comprises decreasing the level of any compound listed in Table 4 or any combination of the 14 compounds listed in Table 4 in the subject. In embodiments, altering the metabolism of a subject comprises decreasing the level of any compound listed in Table 4 or any combination of the 15 compounds listed in Table 4 in the subject. In embodiments, altering the metabolism of a subject comprises decreasing the level of any compound listed in Table 4 or any combination of the 16 compounds listed in Table 4 in the subject. In embodiments, altering the metabolism of a subject comprises decreasing the level of any compound listed in Table 4 or any combination of the 17 compounds listed in Table 4 in the subject. In embodiments, altering the metabolism of a subject comprises decreasing the level of any compound listed in Table 4 or any combination of the 18 compounds listed in Table 4 in the subject. In embodiments, altering the metabolism of a subject comprises decreasing the level of any compound listed in Table 4 or any combination of the 19 compounds listed in Table 4 in the subject. In embodiments, altering the metabolism of a subject comprises decreasing the level of any compound listed in Table 4 or any combination of the 20 compounds listed in Table 4 in the subject. In embodiments, altering the metabolism of a subject comprises decreasing the level of any compound listed in Table 4 or any combination of the 21 compounds listed in Table 4 in the subject.In embodiments, altering the metabolism of the subject comprises decreasing the level of any compound listed in Table 4 or any combination of the 22 compounds listed in Table 4 in the subject. In embodiments, altering the metabolism of the subject comprises decreasing the level of any compound listed in Table 4 or any combination of the 23 compounds listed in Table 4 in the subject. In embodiments, altering the metabolism of the subject comprises decreasing the level of any compound listed in Table 4 or any combination of the 24 compounds listed in Table 4 in the subject. In embodiments, altering the metabolism of the subject comprises decreasing the level of any compound listed in Table 4 or any combination of the 25 compounds listed in Table 4 in the subject. In some embodiments, altering the metabolism of a subject comprises decreasing the level of any compound listed in Table 4 or any combination of the 30 compounds listed in Table 4. In some embodiments, altering the metabolism of a subject comprises decreasing the level of any compound listed in Table 4 or any combination of the 35 compounds listed in Table 4 in the subject. In some embodiments, altering the metabolism of a subject comprises decreasing the level of any compound listed in Table 4 or any combination of the 40 compounds listed in Table 4 in the subject. In some embodiments, altering the metabolism of a subject comprises decreasing the level of any compound listed in Table 4 or any combination of the 45 compounds listed in Table 4 in the subject. In some embodiments, altering the metabolism of a subject comprises decreasing the level of any compound listed in Table 4 or any combination of the 50 compounds listed in Table 4 in the subject. In some embodiments, the level is decreased in the feces of the subject. In some embodiments, the level is decreased in a bodily fluid of the subject.

[0184] In one aspect, a method for treating or preventing an inflammatory disease in a subject in need thereof is provided. The method comprises administering to the subject a therapeutically effective amount of Lactobacillus johnsonii, Faecalibacterium prausnitzii, Akkermansia muciniphila, Myxococcus xanthus, and Pediococcus pentosaceus. In some embodiments, Lactobacillus johnsonii, Faecalibacterium prausnitzii, Akkermansia muciniphila, Myxococcus xanthus, and Pediococcus pentosaceus form the microbial composition provided herein. When Lactobacillus johnsonii, Faecalibacterium prausnitzii, Akkermansia muciniphila, Myxococcus xanthus, and Pediococcus pentosaceus form a microbial composition, the bacteria form part of the composition, including a pharmaceutically acceptable carrier, for administration to or colonization of the intestine. Acceptable carriers include, but are not limited to, inulin. In some embodiments, the intestine is that of a healthy subject. In some embodiments, the intestine is that of a subject in need of treatment or prevention of an inflammatory disease. In some embodiments, the subject is a newborn. As used herein, "newborn" refers to a newborn child or mammal. In some embodiments, the newborn is less than about 4 weeks old.

[0185] In one aspect, a method of treating or preventing an inflammatory disease in a subject in need thereof is provided, comprising administering to the subject an effective amount of a bacterial population comprising Lactobacillus sp., Faecalibacterium sp., Akkermansia sp., Myxococcus sp., and Pediococcus sp.

[0186] In embodiments, the inflammatory disease is selected from the group consisting of allergies, atopy, asthma, autoimmune diseases, autoinflammatory diseases, hypersensitivity, childhood allergic asthma, allergic asthma, inflammatory bowel disease, celiac disease, Crohn's disease, colitis, ulcerative colitis, collagenous colitis, lymphocytic colitis, diverticulitis, irritable bowel syndrome, short bowel syndrome, blind loop syndrome, chronic persistent diarrhea, refractory diarrhea of ​​infancy, traveler's diarrhea, immunoproliferative small bowel disease, chronic prostatitis, post-enteritis syndrome, tropical sprue, Whipple's disease, Wolman's disease, arthritis, rheumatoid arthritis, Behcet's disease, uveitis, pyoderma gangrenosum, and ulcerative colitis. These include erythema nodosum, traumatic brain injury, psoriatic arthritis, juvenile idiopathic arthritis, multiple sclerosis, systemic lupus erythematosus (SLE), myasthenia gravis, juvenile-onset diabetes, type 1 diabetes, Guillain-Barré syndrome, Hashimoto's encephalitis, Hashimoto's thyroiditis, ankylosing spondylitis, psoriasis, Sjögren's syndrome, vasculitis, glomerulonephritis, autoimmune thyroiditis, bullous pemphigoid, sarcoidosis, ichthyosis, Graves' ophthalmopathy, Addison's disease, vitiligo, acne vulgaris, pelvic inflammatory disease, reperfusion injury, sarcoidosis, graft rejection, interstitial cystitis, atherosclerosis, and atopic dermatitis.

[0187] In some embodiments, Lactobacillus johnsonii, Faecalibacterium prausnitzii, Akkermansia muciniphila, Myxococcus xanthus, and Pediococcus pentosaceus are metabolically active. As used herein, "metabolically active" refers to cells (e.g., bacteria) capable of cell division. In some embodiments, metabolically active cells are capable of consuming a substrate (e.g., glucose). In some embodiments, Lactobacillus johnsonii, Faecalibacterium prausnitzii, Akkermansia muciniphila, Myxococcus xanthus, and Pediococcus pentosaceus are metabolically inactive. In some embodiments, the microbial composition is effective for administration to the intestine. In some embodiments, the microbial composition does not include Lactobacillus rhamnosu.

[0188] In embodiments, the microbial composition is effective in increasing an anti-inflammatory metabolite (e.g., a microbial lipid, a microbial carbohydrate, or a microbial amino acid). As described herein, the anti-inflammatory metabolite can be a microbial lipid (e.g., a phospholipid, a polyunsaturated fatty acid). In embodiments, the anti-inflammatory metabolite is a phospholipid. In embodiments, the anti-inflammatory metabolite is a polyunsaturated fatty acid. In embodiments, the anti-inflammatory metabolite is a microbial carbohydrate (e.g., itaconic acid, n-acetylglucosamine, n-acetylgalactosamine, fucosyllactose). In embodiments, the anti-inflammatory metabolite is itaconic acid. In embodiments, the anti-inflammatory metabolite is n-acetylglucosamine. In embodiments, the anti-inflammatory metabolite is n-acetylgalactosamine. In embodiments, the anti-inflammatory metabolite is fucosyllactose. In embodiments, the anti-inflammatory metabolite is a microbial amino acid (e.g., tryptophan). In embodiments, the anti-inflammatory metabolite is tryptophan. The compositions capable of increasing anti-inflammatory metabolites provided herein refer to compositions that result in detectably higher levels of anti-inflammatory metabolites compared to a control. The increased activity may be 10%, 20%, 30%, 40%, 50%, 60%, 70%, 80%, 90% or more higher than the activity in the control. In certain examples, the increase is 1.5-fold, 2-fold, 3-fold, 4-fold, 5-fold, 10-fold or more compared to the control. In several embodiments, the microbial composition is effective in increasing the number of helper T cells that secrete IL-17.

[0189] In embodiments, the microbial composition is effective in reducing pro-inflammatory metabolites. As described herein, the pro-inflammatory metabolite can be a microbial lipid (e.g., dihydroxy-12-octadecenoic acid, cholic acid, or methylmalonic acid). In embodiments, the pro-inflammatory metabolite is dihydroxy-12-octadecenoic acid. In embodiments, the pro-inflammatory metabolite is cholic acid. In embodiments, the pro-inflammatory metabolite is methylmalonic acid. In embodiments, the pro-inflammatory metabolite is a microbial carbohydrate (e.g., n-acetylmuramic acid, lactobionic acid, or maltotriose). In embodiments, the pro-inflammatory metabolite is n-acetylmuramic acid. In embodiments, the pro-inflammatory metabolite is lactobionic acid. In embodiments, the pro-inflammatory metabolite is maltotriose. In embodiments, the pro-inflammatory metabolite is a microbial amino acid (e.g., ornithine or taurine). In embodiments, the pro-inflammatory metabolite is ornithine. In some embodiments, the pro-inflammatory metabolite is taurine. The composition capable of reducing pro-inflammatory metabolites provided herein refers to a composition that results in a detectably lower level of pro-inflammatory metabolites compared to a control. The reduced activity may be 10%, 20%, 30%, 40%, 50%, 60%, 70%, 80%, 90% or less than the activity in the control. In certain instances, the reduction is 1.5-fold, 2-fold, 3-fold, 4-fold, 5-fold, 10-fold or less compared to the control.

[0190] In embodiments, the pro-inflammatory metabolite is IL-4, IL-10, IL-13, or MUC5B. In embodiments, the pro-inflammatory metabolite is IL-4. In embodiments, the pro-inflammatory metabolite is IL-10. In embodiments, the pro-inflammatory metabolite is IL-13. In embodiments, the pro-inflammatory metabolite is MUC5B. In embodiments, the pro-inflammatory metabolite is MUC5AC. In embodiments, the microbial composition is effective in reducing T helper cell type 2 cytokine expression.

[0191] The term "IL-4" as used herein includes any recombinant or naturally occurring form of the interleukin-4 (IL-4) cytokine, or a variant or homolog thereof that maintains the activity of the IL-4 protein (e.g., within at least 50%, 80%, 90%, 95%, 96%, 97%, 98%, 99%, or 100% of the activity compared to IL-4). In some aspects, the variant or homolog has at least 90%, 95%, 96%, 97%, 98%, 99%, or 100% amino acid sequence identity over the entire sequence or a portion of the sequence (e.g., a 50, 100, 150, or 200 contiguous amino acid portion) compared to a naturally occurring IL-4 polypeptide. In several embodiments, the IL-4 is the protein identified by NCBI sequence reference GI:4504669 (Accession No. NP_000580.1; SEQ ID NO: 1), or an isoform, homolog, or functional fragment thereof.

[0192] The term "IL-10" as used herein includes any recombinant or naturally occurring form of interleukin-10 (IL-10) cytokine, or a variant or homolog thereof that maintains the activity of the IL-10 protein (e.g., within at least 50%, 80%, 90%, 95%, 96%, 97%, 98%, 99%, or 100% of the activity compared to IL-10). In some embodiments, the variant or homolog has at least 90%, 95%, 96%, 97%, 98%, 99%, or 100% amino acid sequence identity over the entire sequence or a portion of the sequence (e.g., a 50, 100, 150, or 200 contiguous amino acid portion) compared to a naturally occurring IL-10 polypeptide. In embodiments, the IL-10 is the protein identified by NCBI sequence reference GI:10835141 (Accession No. NP_000563.1; SEQ ID NO:2), or an isoform, homologue, or functional fragment thereof.

[0193] The term "IL-13," as used herein, includes any recombinant or naturally occurring form of interleukin-13 (IL-13) cytokine, or a variant or homolog thereof that maintains the activity of the IL-13 protein (e.g., within at least 50%, 80%, 90%, 95%, 96%, 97%, 98%, 99%, or 100% of the activity compared to IL-13). In some embodiments, the variant or homolog has at least 90%, 95%, 96%, 97%, 98%, 99%, or 100% amino acid sequence identity over the entire sequence or a portion of the sequence (e.g., a 50, 100, 150, or 200 contiguous amino acid portion) compared to a naturally occurring IL-13 polypeptide. In embodiments, the IL-13 is the protein identified by NCBI sequence reference GI:26787978 (Accession No. NP_002179.2; SEQ ID NO:3), or an isoform, homologue, or functional fragment thereof.

[0194] The term "IL-17" as used herein includes any recombinant or naturally occurring form of interleukin-17 (IL-17) cytokine, or a variant or homolog thereof that maintains the activity of the IL-17 protein (e.g., within at least 50%, 80%, 90%, 95%, 96%, 97%, 98%, 99%, or 100% of the activity compared to IL-17). In some aspects, the variant or homolog has at least 90%, 95%, 96%, 97%, 98%, 99%, or 100% amino acid sequence identity over the entire sequence or a portion of the sequence (e.g., a 50, 100, 150, or 200 contiguous amino acid portion) compared to a naturally occurring IL-17 polypeptide. In several embodiments, the IL-17 is the protein identified by UniProt sequence reference Q16552 (SEQ ID NO: 4), or a homolog or functional fragment thereof. In embodiments, the IL-17 is the protein identified by UniProt sequence reference Q9UHF5, or an isoform, homologue, or functional fragment thereof.

[0195] The term "MUC5AC" as used herein includes any recombinant or naturally occurring form of mucin 5AC (MUC5AC) protein, or a variant or homolog thereof that maintains the activity of the MUC5AC protein (e.g., within at least 50%, 80%, 90%, 95%, 96%, 97%, 98%, 99%, or 100% of the activity of MUC5AC). In some aspects, the variant or homolog has at least 90%, 95%, 96%, 97%, 98%, 99%, or 100% amino acid sequence identity over the entire sequence or a portion of the sequence (e.g., a 50, 100, 150, or 200 contiguous amino acid portion) compared to a naturally occurring MUC5AC polypeptide. In several embodiments, MUC5AC is the protein identified by UniProt sequence reference P98088 (SEQ ID NO: 5), or an isoform, homolog, or functional fragment thereof.

[0196] The term "MUC5B" as used herein includes any recombinant or naturally occurring form of mucin 5B (MUC5B) protein, or a variant or homolog thereof that maintains the activity of the MUC5B protein (e.g., within at least 50%, 80%, 90%, 95%, 96%, 97%, 98%, 99%, or 100% of the activity of MUC5B). In some aspects, the variant or homolog has at least 90%, 95%, 96%, 97%, 98%, 99%, or 100% amino acid sequence identity over the entire sequence or a portion of the sequence (e.g., a 50, 100, 150, or 200 contiguous amino acid portion) compared to a naturally occurring MUC5B polypeptide. In several embodiments, MUC5B is the protein identified by UniProt sequence reference Q9HC84 (SEQ ID NO: 6), or an isoform, homolog, or functional fragment thereof.

[0197] In some embodiments, the method further comprises administering a therapeutically effective amount of a fungus. In some embodiments, the fungus is a Malassezia fungus. In some embodiments, the microbial composition is effective in reducing pathogenic fungal activity. "Pathogenic fungal activity," as referred to herein, is metabolic activity derived from a pathogenic fungus. In some embodiments, the pathogenic fungus is Candida albicans. In some embodiments, the pathogenic fungus forms pro-inflammatory lipids.

[0198] In embodiments, the subject is a neonate. In embodiments, the neonate is less than about 4 weeks old. In embodiments, the neonate is treated for at least about 1 month. In embodiments, the neonate is treated for at least about 2 months. In embodiments, the neonate is treated for at least about 3 months. In embodiments, the neonate is treated for at least about 4 months. In embodiments, the neonate is treated for at least about 5 months. In embodiments, the neonate is treated for at least about 6 months.

[0199] In embodiments, the neonate is treated for about 1 month. In embodiments, the neonate is treated for about 2 months. In embodiments, the neonate is treated for about 3 months. In embodiments, the neonate is treated for about 4 months. In embodiments, the neonate is treated for about 5 months. In embodiments, the neonate is treated for about 6 months.

[0200] In embodiments, the neonate is treated for less than about 1 month. In embodiments, the neonate is treated for less than about 2 months. In embodiments, the neonate is treated for less than about 3 months. In embodiments, the neonate is treated for less than about 4 months. In embodiments, the neonate is treated for less than about 5 months. In embodiments, the neonate is treated for less than about 6 months.

[0201] In embodiments, the neonate is treated for about 1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 16, 17, 18, 19, 20, 21, 22, 23, 24, 25, 26, 27, 28, 29, 30, 31, 32, 33, 34, 35, 36, 37, 38, 39, 40, 41, 42, 43, 44, 45, 46, 47, 48, 49, 50, 51, 52, 53, or 54 weeks.

[0202] In embodiments, the inflammatory disease is asthma, ulcerative colitis, irritable bowel syndrome, arthritis, uveitis, pyoderma gangrenosum, or erythema nodosum. In embodiments, the inflammatory disease is asthma. In embodiments, the inflammatory disease is ulcerative colitis. In embodiments, the inflammatory disease is irritable bowel syndrome. In embodiments, the inflammatory disease is arthritis. In embodiments, the inflammatory disease is uveitis. In embodiments, the inflammatory disease is pyoderma gangrenosum. In embodiments, the inflammatory disease is erythema nodosum.

[0203] In one aspect, a method for increasing anti-inflammatory metabolites in a subject in need thereof is provided, the method comprising administering a therapeutically effective amount of Lactobacillus johnsonii, Faecalibacterium prausnitzii, Akkermansia The method includes administering to a subject Lactobacillus johnsonii, Faecalibacterium prausnitzii, Akkermansia muciniphila, Myxococcus xanthus, and Pediococcus pentosaceus. In some embodiments, the method further includes a pharmaceutically active excipient as provided herein. Lactobacillus johnsonii, Faecalibacterium prausnitzii, Akkermansia muciniphila, Myxococcus xanthus, and Pediococcus pentosaceus may form the microbial composition provided herein, including embodiments thereof. Thus, in some embodiments, Lactobacillus johnsonii, Faecalibacterium prausnitzii, Akkermansia muciniphila, Myxococcus xanthus, and Pediococcus pentosaceus form the microbial composition.

[0204] The anti-inflammatory metabolite may be a microbial lipid (e.g., phospholipid, polyunsaturated fatty acid), a microbial carbohydrate (e.g., itaconic acid, n-acetylglucosamine, n-acetylgalactosamine, fucosyllactose), or a microbial amino acid (e.g., tryptophan) as provided herein. In some embodiments, the anti-inflammatory metabolite is a microbial lipid. In some embodiments, the anti-inflammatory metabolite is a microbial carbohydrate. In some embodiments, the anti-inflammatory metabolite is a microbial amino acid.

[0205] In one aspect, a method for reducing pro-inflammatory metabolites in a subject in need thereof is provided. The method includes administering a therapeutically effective amount of Lactobacillus johnsonii, Faecalibacterium prausnitzii, Akkermansia muciniphila, Myxococcus xanthus, and Pediococcus pentosaceus to the subject. In several embodiments, the method further includes a pharmaceutically active excipient provided herein. Lactobacillus johnsonii, Faecalibacterium prausnitzii, Akkermansia muciniphila, Myxococcus xanthus, and Pediococcus pentosaceus, including aspects thereof, may form the microbial composition provided herein. Thus, in embodiments, Lactobacillus johnsonii, Faecalibacterium prausnitzii, Akkermansia muciniphila, Myxococcus xanthus, and Pediococcus pentosaceus form the microbial composition.

[0206] As described herein, the pro-inflammatory metabolite can be a microbial lipid (e.g., dihydroxy-12-octadecenoic acid, cholic acid, or methylmalonic acid). In embodiments, the pro-inflammatory metabolite is dihydroxy-12-octadecenoic acid. In embodiments, the pro-inflammatory metabolite is cholic acid. In embodiments, the pro-inflammatory metabolite is methylmalonic acid. In embodiments, the pro-inflammatory metabolite is a microbial carbohydrate (e.g., n-acetylmuramic acid, lactobionic acid, or maltotriose). In embodiments, the pro-inflammatory metabolite is n-acetylmuramic acid. In embodiments, the pro-inflammatory metabolite is lactobionic acid. In embodiments, the pro-inflammatory metabolite is maltotriose. In embodiments, the pro-inflammatory metabolite is a microbial amino acid (e.g., ornithine or taurine). In embodiments, the pro-inflammatory metabolite is ornithine. In embodiments, the pro-inflammatory metabolite is taurine.

[0207] In certain aspects, methods are provided for increasing levels of anti-inflammatory compounds and / or decreasing levels of pro-inflammatory compounds in a subject in need thereof. In several embodiments, the methods comprise administering to the subject an effective amount of a bacterial population comprising Lactobacillus sp., Faecalibacterium sp., Akkermansia sp., Myxococcus sp., and Pediococcus sp.

[0208] In embodiments, the method for increasing the level of an anti-inflammatory compound increases and / or decreases the level of a pro-inflammatory compound in a subject's feces, blood, plasma, serum, bronchoalveolar lavage fluid, sweat, saliva, sputum, lymph, spinal fluid, urine, tears, bile, aqueous humor, vitreous humor, amniotic fluid, breast milk, cerebrospinal fluid, earwax, nasal mucus, mucus, or sebum.

[0209] In embodiments, the anti-inflammatory compound is a microbial lipid, a microbial carbohydrate, or a microbial amino acid.

[0210] In embodiments, the subject is suffering from a dysbiosis or an inflammatory disease.

[0211] In embodiments, the inflammatory disease is a disease described herein. In embodiments, the inflammatory disease is ulcerative colitis. In embodiments, the inflammatory disease is irritable bowel syndrome. In embodiments, the inflammatory disease is arthritis. In embodiments, the inflammatory disease is uveitis. In embodiments, the inflammatory disease is pyoderma gangrenosum. In embodiments, the inflammatory disease is erythema nodosum.

[0212] In one aspect, a method of treating or preventing a viral respiratory infection in a subject in need thereof is provided, comprising administering to the subject an effective amount of a bacterial population comprising Lactobacillus sp., Faecalibacterium sp., Akkermansia sp., Myxococcus sp., and Pediococcus sp.

[0213] In embodiments, the viral respiratory infection is caused by a respiratory syncytial virus, influenza virus, parainfluenza virus, adenovirus, coronavirus, or rhinovirus. In embodiments, the viral respiratory infection is bronchiolitis, the common cold, croup, or pneumonia.

[0214] In some embodiments, a method of treating or preventing allergies in a subject in need thereof is provided, comprising administering to the subject an effective amount of a bacterial population comprising Lactobacillus sp., Faecalibacterium sp., Akkermansia sp., Myxococcus sp., and Pediococcus sp.

[0215] In embodiments, the allergy is to milk, eggs, fish, shellfish, tree nuts, peanuts, wheat, cat, dog, or rodent dander, insect bites, pollen, latex, dust mites, or soy. In embodiments, the allergy is childhood allergic asthma, hay fever, or allergic airway sensitization. V. Detection Methods

[0216] In one aspect, a method for detecting an anti-inflammatory metabolite in a subject having or at risk of developing an inflammatory disease is provided. The method includes (i) obtaining a biological sample from the subject, and (ii) determining the expression level of the anti-inflammatory metabolite in the biological sample. The anti-inflammatory metabolite can be a microbial lipid (e.g., phospholipid, polyunsaturated fatty acid), a microbial carbohydrate (e.g., itaconic acid, n-acetylglucosamine, n-acetylgalactosamine, fucosyllactose), or a microbial amino acid (e.g., tryptophan) as provided herein. Thus, in some embodiments, the anti-inflammatory metabolite is a microbial lipid or a microbial carbohydrate as described herein. In some embodiments, the anti-inflammatory metabolite is a microbial lipid. In some embodiments, the anti-inflammatory metabolite is a microbial carbohydrate.

[0217] In some embodiments, the expression level of a compound (e.g., a metabolite) is the amount (e.g., weight) of the compound. In some embodiments, the expression level of a compound (e.g., a protein such as a cytokine) is the level of mRNA expression.

[0218] In one aspect, a method for detecting a pro-inflammatory metabolite in a subject having or at risk of developing an inflammatory disease is provided. The method includes (i) obtaining a biological sample from the subject, and (ii) determining the expression level of a pro-inflammatory metabolite in the biological sample. The pro-inflammatory metabolite can be a microbial lipid (e.g., dihydroxy-12-octadecenoic acid, cholic acid, or methylmalonic acid), a microbial carbohydrate (e.g., n-acetylmuramic acid, lactobionic acid, or maltotriose syllactose), or a microbial amino acid (e.g., ornithine or taurine) as provided herein.

[0219] In one aspect, a method for detecting a pro-inflammatory compound in a subject in need thereof is provided, the method comprising: (i) obtaining a biological sample from the subject; and (ii) detecting the pro-inflammatory compound in the biological sample.

[0220] In some aspects, methods for monitoring the effectiveness of a treatment for a dysbiosis or inflammatory disease are provided, which in embodiments include (i) obtaining a biological sample from a subject, and (ii) detecting whether the biological sample is pro-inflammatory.

[0221] In certain aspects, methods for determining inflammatory disease activity in a subject are provided, which in embodiments include (i) obtaining a biological sample from the subject, and (ii) detecting whether the biological sample is pro-inflammatory.

[0222] In certain aspects, methods are provided for detecting anti-inflammatory metabolites in a subject having or at risk of developing an inflammatory disease, hi several embodiments, the methods include (i) obtaining a biological sample from the subject, and (ii) determining the expression level of an anti-inflammatory metabolite in the biological sample.

[0223] In embodiments, the subject has or is at risk of developing a dysbiosis. In embodiments, the subject has an inflammatory disease. In embodiments, the subject is at risk of developing an inflammatory disease.

[0224] In embodiments, the subject (i) has at least one, two, three, or four cousins, grandparents, parents, aunts, uncles, and / or siblings who have been diagnosed with an inflammatory disease; (ii) suffers from constipation, diarrhea, bloating, urgency, and / or abdominal pain; and / or (iii) has received antibiotics within the last 1, 2, or 4 months.

[0225] In embodiments, the inflammatory disease is selected from the group consisting of allergies, atopy, asthma, autoimmune diseases, autoinflammatory diseases, hypersensitivity, childhood allergic asthma, allergic asthma, inflammatory bowel disease, celiac disease, Crohn's disease, colitis, ulcerative colitis, collagenous colitis, lymphocytic colitis, diverticulitis, irritable bowel syndrome, short bowel syndrome, blind loop syndrome, chronic persistent diarrhea, refractory diarrhea of ​​infancy, traveler's diarrhea, immunoproliferative small bowel disease, chronic prostatitis, post-enteritis syndrome, tropical sprue, Whipple's disease, Wolman's disease, arthritis, rheumatoid arthritis, Behcet's disease, uveitis, pyoderma gangrenosum, and ulcerative colitis. These include erythema nodosum, traumatic brain injury, psoriatic arthritis, juvenile idiopathic arthritis, multiple sclerosis, systemic lupus erythematosus (SLE), myasthenia gravis, juvenile-onset diabetes, type 1 diabetes, Guillain-Barré syndrome, Hashimoto's encephalitis, Hashimoto's thyroiditis, ankylosing spondylitis, psoriasis, Sjögren's syndrome, vasculitis, glomerulonephritis, autoimmune thyroiditis, bullous pemphigoid, sarcoidosis, ichthyosis, Graves' ophthalmopathy, Addison's disease, vitiligo, acne vulgaris, pelvic inflammatory disease, reperfusion injury, sarcoidosis, graft rejection, interstitial cystitis, atherosclerosis, and atopic dermatitis.

[0226] In embodiments, the subject is less than about 1, 2, 3, 4, 5, 6, 7, 8, 9, 12, 18, or 24 months old. In embodiments, the subject is less than about 1 month old. In embodiments, the subject is less than 1 month old. In embodiments, the subject is less than about 2 months old. In embodiments, the subject is less than 2 months old. In embodiments, the subject is less than about 3 months old. In embodiments, the subject is less than 3 months old. In embodiments, the subject is less than about 4 months old. In embodiments, the subject is less than 4 months old. In embodiments, the subject is less than about 5 months old. In embodiments, the subject is less than 5 months old. In embodiments, the subject is less than about 6 months old. In embodiments, the subject is less than 6 months old. In embodiments, the subject is less than about 7 months old. In embodiments, the subject is less than 7 months old. In embodiments, the subject is less than about 8 months old. In embodiments, the subject is less than 8 months old. In embodiments, the subject is less than about 9 months old. In embodiments, the subject is less than 9 months old. In embodiments, the subject is less than about 12 months old. In embodiments, the subject is less than 12 months old. In embodiments, the subject is less than about 18 months old. In embodiments, the subject is less than 18 months old. In embodiments, the subject is less than about 24 months old. In embodiments, the subject is less than 24 months old.

[0227] In embodiments, the subject is between about 2 and about 18 years old, or at least about 18 years old. In embodiments, the subject is between about 2 and about 18 years old, or at least 18 years old. In embodiments, the subject is between about 2 and about 18 years old, or at least about 18 years old (e.g., 19, 20, 25, 30, 40, 50, 60, 70, 80, 90) years old. In embodiments, the subject is between about 2 and about 18 years old, or about 19 years old. In embodiments, the subject is between about 2 and about 18 years old, or about 19 years old. In embodiments, the subject is between about 2 and about 18 years old, or about 20 years old. In embodiments, the subject is between about 2 and about 18 years old, or about 20 years old. In embodiments, the subject is between about 2 and about 18 years old, or about 25 years old. In embodiments, the subject is between about 2 and about 18 years old, or about 25 years old. In embodiments, the subject is between about 2 and about 18 years old, or about 30 years old. In embodiments, the subject is between about 2 and about 18 years old, or about 30 years old. In embodiments, the subject is between about 2 and about 18 years old, or about 40 years old. In embodiments, the subject is between about 2 and about 18 years old, or about 40 years old. In embodiments, the subject is between about 2 and about 18 years old, or about 50 years old. In embodiments, the subject is between about 2 and about 18 years old, or about 50 years old. In embodiments, the subject is between about 2 and about 18 years old, or about 60 years old. In embodiments, the subject is between about 2 and about 18 years old, or about 60 years old. In embodiments, the subject is between about 2 and about 18 years old, or about 70 years old. In embodiments, the subject is between about 2 and about 18 years old, or is 70 years old. In embodiments, the subject is between about 2 and about 18 years old, or is about 80 years old. In embodiments, the subject is between about 2 and about 18 years old, or is 80 years old. In embodiments, the subject is between about 2 and about 18 years old, or is about 90 years old. In embodiments, the subject is between about 2 and about 18 years old, or is 90 years old.

[0228] In embodiments, the subject has (a) an increased rate of Streptococcus spp., Bifidobacterium spp., and Enterococcus spp. compared to a healthy or general population; (b) a decreased rate of Alternaria alternata, Aspergillus flavus, Aspergillus cibarius, and Candida sojae compared to a healthy or general population; (c) an increased rate of Candida albicans and Debaryomyces spp. compared to a healthy or general population; (d) a decreased rate of Bifidobacteria spp., Lactobacillus spp., Faecalibacterium spp., and Akkermansia spp. compared to a healthy or general population; (e) a decreased rate of Malassezia spp. compared to a healthy or general population; or (f) a decreased rate of Bacterioides spp., Ruminococcus spp., Prevotella spp. compared to a healthy or general population. or (g) a gastrointestinal microbiome that has an increased proportion of Enterococcus faecalis, Enterococcus faecium, or Clostridium difficile compared to a healthy or general population.

[0229] In some embodiments, the biological sample is a bodily fluid. In some embodiments, the bodily fluid is blood, plasma, serum, fecal fluid, or bronchoalveolar lavage fluid. In some embodiments, the bodily fluid is fecal fluid.

[0230] In some embodiments, detecting the pro-inflammatory compound comprises contacting antigen-presenting cells with the biological sample. In some embodiments, the antigen-presenting cells are dendritic cells. In some embodiments, the dendritic cells are isolated from blood. In some embodiments, the dendritic cells are isolated from blood of a healthy subject (e.g., a subject without an inflammatory disease, an infection, and a subject that has not received antibiotics within about 1, 2, 3, 4, 5, or 6 months). In some embodiments, the dendritic cells are obtained (e.g., isolated, selected, or enriched) from peripheral blood mononuclear cells. In some embodiments, the dendritic cells are part of a primary culture of dendritic cells. In some embodiments, the dendritic cells are part of a culture of dendritic cells that has been passaged less than about 1, 2, 3, 4, 5, 6, 7, 8, 9, or 10 times. In some embodiments, the dendritic cells are not immortalized. In some embodiments, the dendritic cells are immortalized dendritic cells.

[0231] In some embodiments, detecting the pro-inflammatory compound further comprises contacting naive T cells with antigen-presenting cells to generate contacted T cells. In some embodiments, the method further comprises detecting cytokines produced by the contacted T cells and / or progeny of the contacted T cells. In some embodiments, the T cells are isolated from blood. In some embodiments, the T cells are isolated from the blood of a healthy subject (e.g., a subject without an inflammatory disease, an infection, and a subject that has not received antibiotics within about 1, 2, 3, 4, 5, or 6 months). In some embodiments, the T cells are obtained (e.g., isolated, selected, or enriched) from peripheral blood mononuclear cells. In some embodiments, the T cells are part of a primary culture of T cells. In some embodiments, the T cells are part of a culture of T cells that has been passaged less than about 1, 2, 3, 4, 5, 6, 7, 8, 9, or 10 times. In some embodiments, the T cells are not immortalized. In embodiments, the T cells are immortalized T cells.

[0232] In embodiments, a pro-inflammatory compound is detected when: (i) the proportion of T helper (TH)-2 cells is increased in the progeny of the contacted T cells compared to a control; (ii) the proportion of TH-1, TH-17, and / or TH22 cells is increased in the progeny of the contacted T cells compared to a control; (iii) the ratio of TH-1 cells to TH-2 cells is decreased in the progeny of the contacted T cells compared to a control; (iv) the proportion of CD8+ T cells producing IL-17 is increased in the progeny of the contacted T cells compared to a control; and / or (v) the amount of IL-4, IL-10, and / or IL-13 produced by the progeny of the contacted T cells and / or their progeny is increased compared to a control.

[0233] In embodiments, the control is (i) a corresponding proportion, ratio, and / or amount of corresponding T cells and / or their progeny contacted with sterile culture medium; (ii) a corresponding proportion, ratio, and / or amount of corresponding T cells and / or their progeny contacted with antigen-presenting cells that have been contacted with a biological sample from a subject without dysbiosis, inflammatory disease, or gastrointestinal infection; and / or (iii) a reference value corresponding to a proportion, ratio, and / or amount in the general population or a population of subjects without dysbiosis, inflammatory disease, or gastrointestinal infection.

[0234] In embodiments, the method further comprises the step of instructing the subject to undergo treatment or further testing or monitoring for the dysbiosis or inflammatory disease if a pro-inflammatory compound is detected in the subject.

[0235] In embodiments, the method further comprises administering to the subject a composition as described herein, including the embodiments thereof, if a pro-inflammatory compound is detected in the subject.

[0236] In embodiments, the method further comprises diagnosing the subject as having or at risk of developing a dysbiosis or inflammatory disease if a pro-inflammatory compound is detected in the subject.

[0237] In some embodiments, a method for determining whether a subject has or is at risk for developing a dysbiosis or inflammatory disease is provided, which includes (i) obtaining a biological sample from the subject and (ii) detecting a pro-inflammatory compound according to the methods described herein, including in this embodiment.

[0238] In some examples of the disclosed methods, the expression level of an anti-inflammatory or pro-inflammatory metabolite is assessed and compared to a control expression level of the anti-inflammatory or pro-inflammatory metabolite. The control level refers to the expression level of a particular anti-inflammatory or pro-inflammatory metabolite from a sample or subject in the absence of a disease (e.g., inflammatory disease), a selected stage of a disease or condition, or the absence of a specific variable, such as a therapeutic agent. Alternatively, the control level includes a known amount of the anti-inflammatory or pro-inflammatory metabolite. Such a known amount correlates with the average level in subjects in the absence of a disease, a selected stage of a disease or condition, or the absence of a specific variable, such as a therapeutic agent. The control level also includes the expression level of one or more anti-inflammatory or pro-inflammatory metabolites from one or more selected samples or subjects described herein. For example, the control level includes assessing the expression levels of one or more anti-inflammatory or pro-inflammatory metabolites in samples derived from subjects who do not have a disease (e.g., an inflammatory disease), are at a selected stage in the progression of a disease (e.g., an inflammatory disease), or are not receiving treatment for the disease. Another exemplary control level includes assessing the expression levels of one or more anti-inflammatory or pro-inflammatory metabolites in samples obtained from multiple subjects who do not have a disease, are at a selected stage in the progression of a disease, or are not receiving treatment for the disease.

[0239] When the control level includes the expression level of one or more anti-inflammatory or pro-inflammatory metabolites in a sample or subject in the absence of a therapeutic agent (e.g., the microbial composition provided herein, including its embodiments), the control sample or subject is optionally the same sample or subject tested before or after treatment with a therapeutic agent, or a selected sample or subject in the absence of a therapeutic agent. Alternatively, the control level is the average expression level calculated from several subjects who do not have a particular disease. Control levels also include known control levels or values ​​known in the art.

[0240] In embodiments, the biological sample is a bodily fluid. In embodiments, the bodily fluid is serum, fecal fluid, or bronchoalveolar lavage fluid. In embodiments, the bodily fluid is serum. In embodiments, the bodily fluid is fecal fluid. In embodiments, the bodily fluid is bronchoalveolar lavage fluid. In embodiments, the biological sample is tissue. In embodiments, the tissue is lung, spleen, or ileum tissue. In embodiments, the biological sample is cells. In embodiments, the biological sample is lung cells. In embodiments, the biological sample is spleen cells. In embodiments, the biological sample is ileum cells. In embodiments, the sample is one or more bacterial cells.

[0241] In some embodiments, the biological sample is a bodily fluid obtained by filtration and / or centrifugation. For example, the biological sample can be, for example, a blood or fecal filtrate or a centrifuged blood or fecal supernatant. In some embodiments, the filtrate is centrifuged. In some embodiments, the supernatant is filtered. In some embodiments, centrifugation is used to increase the fluid passing through the filter. Non-limiting examples of filters include filters that restrict any molecules having a diameter (or average diameter) greater than 50, 100, 200, 300, 400, 500, 50-500, 50-100, 100-500 nm, or a diameter (e.g., average diameter) greater than 0.5, 1, 1.5, 2, 2.5, 5, 10, 15, 25, 50, 100, or 200 microns. In embodiments, the filter has pores about 50, 100, 200, 300, 400, 500, 50-500, 50-100, 100-500 nm in diameter or about 0.5, 1, 1.5, 2, 2.5, 5, 10, 15, 25, 50, 100, or 200 microns in diameter.

[0242] In embodiments, detecting the compound (e.g., metabolite) and / or its expression level comprises high performance liquid chromatography (HPLC), gas chromatography, liquid chromatography, mass spectrometry (MS), inductively coupled plasma mass spectrometry (ICP-MS), accelerator mass spectrometry (AMS), thermal ionization mass spectrometry (TIMS) and spark source mass spectrometry (SSMS), matrix-assisted laser desorption / ionization (MALDI), and / or MALDI-TOF.

[0243] In some embodiments, detecting the expression level of the compound comprises lysing the cells, hi some embodiments, detecting the expression level of the compound comprises polymerase chain reaction (e.g., reverse transcriptase polymerase chain reaction), microarray analysis, immunohistochemistry, or flow cytometry.

[0244] In some embodiments, the determining step comprises: (a) contacting the anti-inflammatory metabolite with an antigen-presenting cell in vitro, thereby forming a metabolite-antigen-presenting cell; (b) contacting the metabolite-antigen-presenting cell with a T cell, thereby forming a contacted T cell; and (c) detecting cytokines produced by the contacted T cell. In some embodiments, the cytokines are produced by activated or differentiating T cells.

[0245] In several embodiments, the determining step comprises: (a) contacting the pro-inflammatory metabolite with an antigen-presenting cell in vitro, thereby forming a metabolite-antigen-presenting cell; (b) contacting the metabolite-antigen-presenting cell with a T cell, thereby forming a contacted T cell; and (c) detecting cytokines produced by the contacted T cell.

[0246] In embodiments, the inflammatory disease is asthma, ulcerative colitis, irritable bowel syndrome, arthritis, uveitis, pyoderma gangrenosum, or erythema nodosum. In embodiments, the inflammatory disease is asthma. In embodiments, the inflammatory disease is ulcerative colitis. In embodiments, the inflammatory disease is irritable bowel syndrome. In embodiments, the inflammatory disease is arthritis. In embodiments, the inflammatory disease is uveitis. In embodiments, the inflammatory disease is pyoderma gangrenosum. In embodiments, the inflammatory disease is erythema nodosum.

[0247] In one aspect, a method of determining whether a subject has or is at risk of developing an inflammatory disease is provided, comprising: (i) detecting the expression level of one or more anti-inflammatory or pro-inflammatory metabolites in the subject; (ii) determining whether the expression level is elevated or decreased relative to a standard control, wherein an elevated expression level of a pro-inflammatory metabolite or a decreased expression level of an anti-inflammatory metabolite relative to the standard control indicates that the subject has or is at risk of developing an inflammatory disease; and (iii) determining whether the subject has or is at risk of developing an inflammatory disease based at least in part on the expression levels in step (ii).

[0248] In one aspect, a method of determining whether a subject has or is at risk of developing an inflammatory disease is provided, comprising: (i) detecting an expression level of one or more pro-inflammatory metabolites in the subject; (ii) determining whether the expression level is elevated or decreased relative to a standard control, wherein an elevated expression level of a pro-inflammatory metabolite relative to the standard control indicates that the subject has or is at risk of developing an inflammatory disease; and (iii) determining whether the subject has or is at risk of developing an inflammatory disease based at least in part on the expression level in step (ii).

[0249] In another aspect, a method of determining whether a subject has or is at risk of developing an inflammatory disease is provided, comprising: (i) detecting an expression level of one or more anti-inflammatory metabolites in the subject; (ii) determining whether the expression level is elevated or decreased relative to a standard control, wherein a decreased expression level of the anti-inflammatory metabolite relative to the standard control indicates that the subject has or is at risk of developing an inflammatory disease; and (iii) determining whether the subject has or is at risk of developing an inflammatory disease based at least in part on the expression level in step (ii).

[0250] In several embodiments, the anti-inflammatory metabolite is a microbial lipid, a microbial carbohydrate, or a microbial amino acid as provided herein. The anti-inflammatory metabolite can be a microbial lipid (e.g., phospholipid, polyunsaturated fatty acid), a microbial carbohydrate (e.g., itaconic acid, n-acetylglucosamine, n-acetylgalactosamine, fucosyllactose), or a microbial amino acid (e.g., tryptophan) as provided herein. In several embodiments, the anti-inflammatory metabolite is a microbial lipid. In several embodiments, the anti-inflammatory metabolite is a microbial carbohydrate. In several embodiments, the anti-inflammatory metabolite is a microbial amino acid.

[0251] In some embodiments, the pro-inflammatory metabolite is a microbial lipid, microbial carbohydrate, or microbial amino acid as provided herein. The pro-inflammatory metabolite can be a microbial lipid (e.g., dihydroxy-12-octadecenoic acid, cholic acid, or methylmalonic acid), a microbial carbohydrate (e.g., n-acetylmuramic acid, lactobionic acid, or maltotriose syllactose), or a microbial amino acid (e.g., ornithine or taurine) as provided herein.

[0252] In embodiments, the inflammatory disease is asthma, ulcerative colitis, irritable bowel syndrome, arthritis, uveitis, pyoderma gangrenosum, or erythema nodosum. In embodiments, the inflammatory disease is asthma. In embodiments, the inflammatory disease is ulcerative colitis. In embodiments, the inflammatory disease is irritable bowel syndrome. In embodiments, the inflammatory disease is arthritis. In embodiments, the inflammatory disease is uveitis. In embodiments, the inflammatory disease is pyoderma gangrenosum. In embodiments, the inflammatory disease is erythema nodosum.

[0253] In one aspect, a method for monitoring the effect of treatment on an inflammatory disease in a subject undergoing treatment or a patient treated for an inflammatory disease is provided, comprising the steps of (i) determining a first expression level of an anti-inflammatory metabolite in the subject at a first time point, (ii) determining a second expression level of the anti-inflammatory metabolite in the subject at a second time point, and (iii) comparing the second expression level of the anti-inflammatory metabolite to the first expression level of the anti-inflammatory metabolite, thereby determining the effect of treatment on the inflammatory disease in the subject.

[0254] In embodiments, the anti-inflammatory metabolite is a microbial lipid, microbial carbohydrate, or microbial amino acid as provided herein. In embodiments, the anti-inflammatory metabolite is a microbial lipid. In embodiments, the anti-inflammatory metabolite is a microbial carbohydrate. In embodiments, the anti-inflammatory metabolite is a microbial amino acid.

[0255] In one aspect, a method of monitoring the effect of treatment on an inflammatory disease in a subject undergoing treatment or a patient treated for an inflammatory disease is provided, the method comprising the steps of (i) determining a first expression level of a pro-inflammatory metabolite in the subject at a first time point, (ii) determining a second expression level of the pro-inflammatory metabolite in the subject at a second time point, and (iii) comparing the second expression level of the pro-inflammatory metabolite to the first expression level of the pro-inflammatory metabolite, thereby determining the effect of treatment on the inflammatory disease in the subject.

[0256] In embodiments, the pro-inflammatory metabolite is a microbial lipid, microbial carbohydrate, or microbial amino acid as provided herein. In embodiments, the pro-inflammatory metabolite is a microbial lipid. In embodiments, the pro-inflammatory metabolite is a microbial carbohydrate. In embodiments, the pro-inflammatory metabolite is a microbial amino acid.

[0257] In embodiments, the inflammatory disease is asthma, ulcerative colitis, irritable bowel syndrome, arthritis, uveitis, pyoderma gangrenosum, or erythema nodosum. In embodiments, the inflammatory disease is asthma. In embodiments, the inflammatory disease is ulcerative colitis. In embodiments, the inflammatory disease is irritable bowel syndrome. In embodiments, the inflammatory disease is arthritis. In embodiments, the inflammatory disease is uveitis. In embodiments, the inflammatory disease is pyoderma gangrenosum. In embodiments, the inflammatory disease is erythema nodosum.

[0258] In one aspect, a method of determining whether a subject has or is at risk for developing a dysbiosis or inflammatory disease is provided, the method comprising (i) obtaining a biological sample from the subject, and (ii) detecting whether the biological sample is pro-inflammatory.

[0259] In embodiments, the subject has or lives with someone who has a bacterial, viral, or fungal gastrointestinal infection.

[0260] In embodiments, the subject (i) has at least one, two, three, or four cousins, grandparents, parents, aunts, uncles, and / or siblings who have been diagnosed with an inflammatory disease; (ii) suffers from constipation, diarrhea, bloating, urgency, and / or abdominal pain; and / or (iii) has received antibiotics within the last 1, 2, or 4 months.

[0261] In embodiments, the inflammatory disease is selected from the group consisting of allergies, atopy, asthma, autoimmune diseases, autoinflammatory diseases, hypersensitivity, childhood allergic asthma, allergic asthma, inflammatory bowel disease, celiac disease, Crohn's disease, colitis, ulcerative colitis, collagenous colitis, lymphocytic colitis, diverticulitis, irritable bowel syndrome, short bowel syndrome, blind loop syndrome, chronic persistent diarrhea, refractory diarrhea of ​​infancy, traveler's diarrhea, immunoproliferative small bowel disease, chronic prostatitis, post-enteritis syndrome, tropical sprue, Whipple's disease, Wolman's disease, arthritis, rheumatoid arthritis, Behcet's disease, uveitis, pyoderma gangrenosum, and ulcerative colitis. These include erythema nodosum, traumatic brain injury, psoriatic arthritis, juvenile idiopathic arthritis, multiple sclerosis, systemic lupus erythematosus (SLE), myasthenia gravis, juvenile-onset diabetes, type 1 diabetes, Guillain-Barré syndrome, Hashimoto's encephalitis, Hashimoto's thyroiditis, ankylosing spondylitis, psoriasis, Sjögren's syndrome, vasculitis, glomerulonephritis, autoimmune thyroiditis, bullous pemphigoid, sarcoidosis, ichthyosis, Graves' ophthalmopathy, Addison's disease, vitiligo, acne vulgaris, pelvic inflammatory disease, reperfusion injury, sarcoidosis, graft rejection, interstitial cystitis, atherosclerosis, and atopic dermatitis.

[0262] In embodiments, the subject is less than about 1, 2, 3, 4, 5, 6, 7, 8, 9, 12, 18, or 24 months old. In embodiments, the subject is less than about 1 month old. In embodiments, the subject is less than 1 month old. In embodiments, the subject is less than about 2 months old. In embodiments, the subject is less than 2 months old. In embodiments, the subject is less than about 3 months old. In embodiments, the subject is less than 3 months old. In embodiments, the subject is less than about 4 months old. In embodiments, the subject is less than 4 months old. In embodiments, the subject is less than about 5 months old. In embodiments, the subject is less than 5 months old. In embodiments, the subject is less than about 6 months old. In embodiments, the subject is less than 6 months old. In embodiments, the subject is less than about 7 months old. In embodiments, the subject is less than 7 months old. In embodiments, the subject is less than about 8 months old. In embodiments, the subject is less than 8 months old. In embodiments, the subject is less than about 9 months old. In embodiments, the subject is less than 9 months old. In embodiments, the subject is less than about 12 months old. In embodiments, the subject is less than 12 months old. In embodiments, the subject is less than about 18 months old. In embodiments, the subject is less than 18 months old. In embodiments, the subject is less than about 24 months old. In embodiments, the subject is less than 24 months old.

[0263] In embodiments, the subject is between about 2 and about 18 years old, or at least about 18 years old. In embodiments, the subject is between about 2 and about 18 years old, or at least 18 years old. In embodiments, the subject is between about 2 and about 18 years old, or at least about 18 years old (e.g., 19, 20, 25, 30, 40, 50, 60, 70, 80, 90) years old. In embodiments, the subject is between about 2 and about 18 years old, or about 19 years old. In embodiments, the subject is between about 2 and about 18 years old, or about 19 years old. In embodiments, the subject is between about 2 and about 18 years old, or about 20 years old. In embodiments, the subject is between about 2 and about 18 years old, or about 20 years old. In embodiments, the subject is between about 2 and about 18 years old, or about 25 years old. In embodiments, the subject is between about 2 and about 18 years old, or about 25 years old. In embodiments, the subject is between about 2 and about 18 years old, or about 30 years old. In embodiments, the subject is between about 2 and about 18 years old, or about 30 years old. In embodiments, the subject is between about 2 and about 18 years old, or about 40 years old. In embodiments, the subject is between about 2 and about 18 years old, or about 40 years old. In embodiments, the subject is between about 2 and about 18 years old, or about 50 years old. In embodiments, the subject is between about 2 and about 18 years old, or about 50 years old. In embodiments, the subject is between about 2 and about 18 years old, or about 60 years old. In embodiments, the subject is between about 2 and about 18 years old, or about 60 years old. In embodiments, the subject is between about 2 and about 18 years old, or about 70 years old. In embodiments, the subject is between about 2 and about 18 years old, or is 70 years old. In embodiments, the subject is between about 2 and about 18 years old, or is about 80 years old. In embodiments, the subject is between about 2 and about 18 years old, or is 80 years old. In embodiments, the subject is between about 2 and about 18 years old, or is about 90 years old. In embodiments, the subject is between about 2 and about 18 years old, or is 90 years old.

[0264] In embodiments, the subject has (a) an increased rate of Streptococcus spp., Bifidobacterium spp., and Enterococcus spp. compared to a healthy or general population; (b) a decreased rate of Alternaria alternata, Aspergillus flavus, Aspergillus cibarius, and Candida sojae compared to a healthy or general population; (c) an increased rate of Candida albicans and Debaryomyces spp. compared to a healthy or general population; (d) a decreased rate of Bifidobacteria spp., Lactobacillus spp., Faecalibacterium spp., and Akkermansia spp. compared to a healthy or general population; (e) a decreased rate of Malassezia spp. compared to a healthy or general population; or (f) a decreased rate of Bacterioides spp., Ruminococcus spp., Prevotella spp. compared to a healthy or general population. or (g) a gastrointestinal microbiome that has an increased proportion of Enterococcus faecalis, Enterococcus faecium, or Clostridium difficile compared to a healthy or general population.

[0265] In some embodiments, the biological sample is a bodily fluid. In some embodiments, the bodily fluid is blood, plasma, serum, fecal fluid, or bronchoalveolar lavage fluid. In some embodiments, the bodily fluid is fecal fluid.

[0266] In embodiments, the step of detecting whether the biological sample is pro-inflammatory comprises contacting an antigen-presenting cell with the biological sample, hi embodiments, the antigen-presenting cell is a dendritic cell.

[0267] In embodiments, the step of detecting whether the biological sample is pro-inflammatory further comprises contacting naive T cells with antigen-presenting cells to generate contacted T cells.

[0268] In embodiments, the method further comprises detecting cytokines produced by the contacted T cell and / or progeny of the contacted T cell.

[0269] In embodiments, the biological sample is detected to be pro-inflammatory if: (i) the proportion of T helper (TH)-2 cells is increased in the progeny of the contacted T cells compared to a control; (ii) the proportion of TH-1, TH-17, and / or TH22 cells is increased in the progeny of the contacted T cells compared to a control; (iii) the ratio of TH-1 cells to TH-2 cells is decreased in the progeny of the contacted T cells compared to a control; (iv) the proportion of CD8+ T cells that produce IL-17 is increased in the progeny of the contacted T cells compared to a control; and / or (v) the amount of IL-4, IL-10, and / or IL-13 produced by the progeny of the contacted T cells and / or their progeny is increased compared to a control.

[0270] In embodiments, the control is (i) a corresponding proportion, ratio, and / or amount of corresponding T cells and / or their progeny contacted with sterile culture medium; (ii) a corresponding proportion, ratio, and / or amount of corresponding T cells and / or their progeny contacted with antigen-presenting cells that have been contacted with a biological sample from a subject without dysbiosis, inflammatory disease, or gastrointestinal infection; and / or (iii) a reference value corresponding to a proportion, ratio, and / or amount in the general population or a population of subjects without dysbiosis, inflammatory disease, or gastrointestinal infection.

[0271] In embodiments, the method further comprises the step of instructing the subject to undergo treatment or further testing or monitoring for the dysbiosis or inflammatory disease if the biological sample is detected to be pro-inflammatory.

[0272] In several embodiments, the method further comprises administering to the subject a bacterial population or composition described herein, including the embodiments thereof, if the biological sample is detected to be pro-inflammatory.

[0273] In embodiments, the subject has (a) an increased rate of Streptococcus spp., Bifidobacterium spp., and Enterococcus spp. compared to a healthy or general population; (b) a decreased rate of Alternaria alternata, Aspergillus flavus, Aspergillus cibarius, and Candida sojae compared to a healthy or general population; (c) an increased rate of Candida albicans and Debaryomyces spp. compared to a healthy or general population; (d) a decreased rate of Bifidobacteria spp., Lactobacillus spp., Faecalibacterium spp., and Akkermansia spp. compared to a healthy or general population; (e) a decreased rate of Malassezia spp. compared to a healthy or general population; or (f) a decreased rate of Bacterioides spp., Ruminococcus spp., Prevotella spp. compared to a healthy or general population. or (g) a gastrointestinal microbiome that has an increased proportion of Enterococcus faecalis, Enterococcus faecium, or Clostridium difficile compared to a healthy or general population.

[0274] In embodiments, the method comprises determining whether the subject has: (a) increased rates of Streptococcus spp., Bifidobacterium spp., and Enterococcus spp. compared to a healthy or general population; (b) decreased rates of Alternaria alternata, Aspergillus flavus, Aspergillus cibarius, and Candida sojae compared to a healthy or general population; or (c) decreased rates of Candida sojae compared to a healthy or general population. (d) decreased rates of Bifidobacteria spp., Lactobacillus spp., Faecalibacterium spp., and Akkermansia spp. compared to the healthy or general population; (e) decreased rates of Malassezia spp. compared to the healthy or general population; (f) decreased rates of Bacterioides spp., Ruminococcus spp. compared to the healthy or general population. or Bifidobacterium spp.; or (g) a gastrointestinal microbiome that has an increased proportion of Enterococcus faecalis, Enterococcus faecium, or Clostridium difficile compared to a healthy or general population.

[0275] In embodiments, a method of treating or preventing a dysbiosis, a viral respiratory infection, or an inflammatory disease in a subject determined to have or be at risk of developing a dysbiosis, a viral respiratory infection, or an inflammatory disease according to the methods described herein, including embodiments thereof, hi embodiments, the method comprises administering to the subject a population of bacteria disclosed herein.

[0276] In another aspect, a method for determining inflammatory disease activity in a subject is provided, the method comprising: (i) detecting an expression level of one or more anti-inflammatory metabolites in the subject; (ii) determining whether the expression level is modulated compared to a standard control, thereby determining the inflammatory disease activity in the subject; and (iii) determining the inflammatory disease activity in the subject based at least in part on the expression level in step (ii).

[0277] In embodiments, the anti-inflammatory metabolite is a microbial lipid, microbial carbohydrate, or microbial amino acid as provided herein. In embodiments, the anti-inflammatory metabolite is a microbial lipid. In embodiments, the anti-inflammatory metabolite is a microbial carbohydrate. In embodiments, the anti-inflammatory metabolite is a microbial amino acid.

[0278] In another aspect, a method for determining inflammatory disease activity in a subject is provided, comprising: (i) detecting an expression level of one or more pro-inflammatory metabolites in the subject; (ii) determining whether the expression level is modulated compared to a standard control, thereby determining inflammatory disease activity in the subject; and (iii) determining inflammatory disease activity in the subject based at least in part on the expression level in step (ii).

[0279] In embodiments, the pro-inflammatory metabolite is a microbial lipid, microbial carbohydrate, or microbial amino acid as provided herein. In embodiments, the anti-inflammatory metabolite is a microbial lipid. In embodiments, the anti-inflammatory metabolite is a microbial carbohydrate. In embodiments, the anti-inflammatory metabolite is a microbial amino acid.

[0280] In embodiments, the inflammatory disease is asthma, ulcerative colitis, irritable bowel syndrome, arthritis, uveitis, pyoderma gangrenosum, or erythema nodosum. In embodiments, the inflammatory disease is asthma. In embodiments, the inflammatory disease is ulcerative colitis. In embodiments, the inflammatory disease is irritable bowel syndrome. In embodiments, the inflammatory disease is arthritis. In embodiments, the inflammatory disease is uveitis. In embodiments, the inflammatory disease is pyoderma gangrenosum. In embodiments, the inflammatory disease is erythema nodosum.

[0281] In one aspect, a method for determining whether a subject has or is at risk for developing a dysbiosis or inflammatory disease is provided, comprising: (i) detecting the expression level of one or more anti-inflammatory or pro-inflammatory metabolites in the subject; (ii) determining whether the expression level is elevated or decreased relative to a standard control, wherein an elevated expression level of a pro-inflammatory metabolite or a decreased expression level of an anti-inflammatory metabolite relative to the standard control indicates that the subject has or is at risk for developing an inflammatory disease; and (iii) determining whether the subject has or is at risk for developing an inflammatory disease based at least in part on the expression levels in step (ii).

[0282] In certain aspects, methods are provided for monitoring the effect of treatment on an inflammatory disease in a subject undergoing treatment for or a patient treated for an inflammatory disease, the methods comprising: (i) determining a first expression level of an anti-inflammatory or pro-inflammatory metabolite in the subject at a first time point; (ii) determining a second expression level of the anti-inflammatory or pro-inflammatory metabolite in the subject at a second time point; and (iii) comparing the second expression level of the anti-inflammatory or pro-inflammatory metabolite to the first expression level of the anti-inflammatory or pro-inflammatory metabolite, thereby determining the effect of treatment on the inflammatory disease in the subject.

[0283] In one aspect, a method for determining inflammatory disease activity in a subject is provided, the method comprising: (i) detecting the expression level of one or more anti-inflammatory or pro-inflammatory metabolites in the subject; (ii) determining whether the expression level is modulated compared to a standard control, thereby determining the inflammatory disease activity in the subject; and (iii) determining the inflammatory disease activity in the subject based at least in part on the expression level in step (ii).

[0284] [Table 1-1] [Table 1-2] [Table 1-3] [Table 1-4]

[0285] It is understood that the examples and embodiments described herein are for illustrative purposes only, and that various modifications or variations in light thereof will occur to those skilled in the art and are within the spirit and scope of this application and the scope of the appended claims. All publications, patents, and patent applications cited herein are hereby incorporated by reference in their entirety for all purposes. Embodiment

[0286] The embodiment includes the following P1 to P34.

[0287] Embodiment P1. A method of treating or preventing an inflammatory disease in a subject in need thereof, comprising administering to the subject a therapeutically effective amount of Lactobacillus johnsonii, Faecalibacterium prausnitzii, Akkermansia muciniphila, Myxococcus xanthus, and Pediococcus pentosaceus.

[0288] Embodiment P2. The method of embodiment 1, further comprising a pharmaceutically active excipient.

[0289] Embodiment P3. The method of embodiment 1 or 2, wherein said Lactobacillus johnsonii, Faecalibacterium prausnitzii, Akkermansia muciniphila, Myxococcus xanthus, and Pediococcus pentosaceus form a microbial composition.

[0290] Embodiment P4. The method of embodiment 3, wherein the microbial composition is effective for administration to the intestine.

[0291] Embodiment P5. The method of embodiment 3, wherein the microbial composition is effective to increase anti-inflammatory metabolites.

[0292] Embodiment P6. The method of embodiment 3, wherein the microbial composition is effective to reduce pro-inflammatory metabolites.

[0293] Embodiment P7. The method of embodiment 5, wherein the anti-inflammatory metabolite is a microbial lipid, a microbial carbohydrate, or a microbial amino acid.

[0294] Embodiment P8. The method of embodiment 6, wherein the pro-inflammatory metabolite is a microbial lipid, a microbial carbohydrate, or a microbial amino acid.

[0295] Embodiment P9. The method of embodiment 8, wherein the pro-inflammatory metabolite is IL-4, IL-10, IL-13, or MUC5B.

[0296] Embodiment P10. The Lactobacillus johnsonii, Faecalibacterium prausnitzii, Akkermansia muciniphila, Myxococcus xanthus and Pediococcus 10. The method of one of embodiments 1 or 9, wherein the pentosaceus is metabolically active.

[0297] Embodiment P11. The Lactobacillus johnsonii, Faecalibacterium prausnitzii, Akkermansia muciniphila, Myxococcus xanthus and Pediococcus 10. The method of one of embodiments 1 or 9, wherein the pentosaceus is metabolically inactive.

[0298] Embodiment P12. The method of one of embodiments 1 to 11, further comprising administering a therapeutically effective amount of a fungus.

[0299] Embodiment P13. The method of one of embodiments 1 to 12, wherein the subject is a newborn.

[0300] Embodiment P14. The method of one of embodiments 1-13, wherein the inflammatory disease is asthma, ulcerative colitis, irritable bowel syndrome, arthritis, uveitis, pyoderma gangrenosum, or erythema nodosum.

[0301] Embodiment P15. A method of increasing anti-inflammatory metabolites in a subject in need thereof, comprising administering to the subject a therapeutically effective amount of Lactobacillus johnsonii, Faecalibacterium prausnitzii, Akkermansia muciniphila, Myxococcus xanthus, and Pediococcus pentosaceus.

[0302] Embodiment P16. The method of embodiment 15, further comprising a pharmaceutically active excipient.

[0303] Embodiment P17. Said Lactobacillus johnsonii, Faecalibacterium prausnitzii, Akkermansia muciniphila, Myxococcus xanthus and Pediococcus 17. The method of embodiment 15 or 16, wherein S. pentosaceus forms the microbial composition.

[0304] Embodiment P18. The method of one of embodiments 15 to 17, wherein the anti-inflammatory metabolite is a microbial lipid, a microbial carbohydrate, or a microbial amino acid.

[0305] Embodiment P19. The method of one of embodiments 15-18, wherein the inflammatory disease is asthma, ulcerative colitis, irritable bowel syndrome, arthritis, uveitis, pyoderma gangrenosum, or erythema nodosum.

[0306] Embodiment P20. A method for detecting an anti-inflammatory metabolite in a subject having or at risk of developing an inflammatory disease, comprising: (i) obtaining a biological sample from the subject; and (ii) determining the expression level of an anti-inflammatory metabolite in the biological sample.

[0307] Embodiment P21. The method of embodiment 20, wherein the anti-inflammatory metabolite is a microbial lipid or a microbial carbohydrate.

[0308] Embodiment P22. The method of embodiment 20 or 21, wherein the biological sample is a body fluid.

[0309] Embodiment P23. The method of embodiment 22, wherein said bodily fluid is serum, fecal fluid, or bronchoalveolar lavage fluid.

[0310] Embodiment P24. The method of one of embodiments 20 to 23, wherein said determining step comprises (a) contacting the anti-inflammatory metabolite with an antigen-presenting cell in vitro, thereby forming a metabolite-antigen-presenting cell; (b) contacting the metabolite-antigen-presenting cell with a T cell, thereby forming a contacted T cell; and (c) detecting cytokines produced by the contacted T cell.

[0311] Embodiment P25. The method of one of embodiments 20-24, wherein the inflammatory disease is asthma, ulcerative colitis, irritable bowel syndrome, arthritis, uveitis, pyoderma gangrenosum, or erythema nodosum.

[0312] Embodiment P26. A method for determining whether a subject has or is at risk of developing an inflammatory disease, the method comprising the steps of: (i) detecting expression levels of one or more anti-inflammatory or pro-inflammatory metabolites in the subject; (ii) determining whether the expression levels are elevated or decreased relative to a standard control, wherein an elevated expression level of a pro-inflammatory metabolite or a decreased expression level of an anti-inflammatory metabolite relative to the standard control indicates that the subject has or is at risk of developing an inflammatory disease; and (iii) determining whether the subject has or is at risk of developing an inflammatory disease based at least in part on the expression levels in step (ii).

[0313] Embodiment P27. The method of embodiment 26, wherein the inflammatory disease is asthma, ulcerative colitis, irritable bowel syndrome, arthritis, uveitis, pyoderma gangrenosum, or erythema nodosum.

[0314] Embodiment P28. The method of embodiment 26, wherein the anti-inflammatory metabolite is a microbial lipid, a microbial carbohydrate, or a microbial amino acid.

[0315] Embodiment P29. A method of monitoring the effect of treatment on an inflammatory disease in a subject being treated for or a patient who has been treated for an inflammatory disease, the method comprising: (i) determining a first expression level of an anti-inflammatory metabolite in the subject at a first time point; (ii) determining a second expression level of an anti-inflammatory metabolite in the subject at a second time point; and (iii) comparing the second expression level of an anti-inflammatory metabolite with the first expression level of an anti-inflammatory metabolite, thereby determining the effect of treatment on the inflammatory disease in the subject.

[0316] Embodiment P30. The method of embodiment 29, wherein said inflammatory disease is asthma, ulcerative colitis, irritable bowel syndrome, arthritis, uveitis, pyoderma gangrenosum, or erythema nodosum.

[0317] Embodiment P31. The method of embodiment 29, wherein the anti-inflammatory metabolite is a microbial lipid, a microbial carbohydrate, or a microbial amino acid.

[0318] Embodiment P32. A method of determining inflammatory disease activity in a subject, the method comprising the steps of: (i) detecting an expression level of one or more anti-inflammatory metabolites in the subject; (ii) determining whether the expression level is modulated compared to a standard control, thereby determining inflammatory disease activity in the subject; and (iii) determining the inflammatory disease activity in the subject based at least in part on the expression level in step (ii).

[0319] Embodiment P33. The method of embodiment 32, wherein said inflammatory disease is asthma, ulcerative colitis, irritable bowel syndrome, arthritis, uveitis, pyoderma gangrenosum, or erythema nodosum.

[0320] Embodiment P34. The method of embodiment 32, wherein the anti-inflammatory metabolite is a microbial lipid, a microbial carbohydrate, or a microbial amino acid.

[0321] Further embodiments include the following embodiments 1-111.

[0322] Embodiment 1. A method of treating or preventing dysbiosis in a subject in need thereof, comprising administering to the subject an effective amount of a bacterial population comprising Lactobacillus sp., Faecalibacterium sp., Akkermansia sp., Myxococcus sp., and Pediococcus sp.

[0323] Embodiment 2. The method of embodiment 1, wherein (i) the Lactobacillus sp. is Lactobacillus johnsonii, (ii) the Faecalibacterium sp. is Faecalibacterium prausnitzii, (iii) the Akkermansia sp. is Akkermansia muciniphila, (iv) the Myxococcus sp. is Myxococcus xanthus, and (v) the Pediococcus sp. is Pediococcus pentosaceus.

[0324] Embodiment 3. (i) The Lactobacillus sp. is Lactobacillus zeae, Lactobacillus acidipiscis, Lactobacillus acidophilus, Lactobacillus agilis, Lactobacillus aviarius, Lactobacillus brevis, Lactobacillus coleohominis, Lactobacillus crispatus, Lactobacillus crustorum, Lactobacillus curvatus, Lactobacillus diolivorans, Lactobacillus farraginis, Lactobacillus fermentum, Lactobacillus fuchuensis, Lactobacillus harbinensis, Lactobacillus helveticus, Lactobacillus hilgardii, Lactobacillus intestinalis, Lactobacillus jensenii, Lactobacillus kefiranofaciens, Lactobacillus kefiri, Lactobacillus lindneri, Lactobacillus mali, Lactobacillus manihotivorans, Lactobacillus mucosae, Lactobacillus oeni, Lactobacillus oligofermentans, Lactobacillus panis, Lactobacillus pantheris, Lactobacillus parabrevis, Lactobacillus paracollinoides, Lactobacillus parakefiri, Lactobacillus paraplantarum, Lactobacillus pentosus, Lactobacillus pontis, Lactobacillus reuteri, Lactobacillus rossiae, Lactobacillus salivarius, Lactobacillus siliginis, Lactobacillus sucicola, Lactobacillus vaccinostercus, Lactobacillus vaginalis, Lactobacillus vini, Lactococcus garvieae, or Lactococcus lactis, (ii) the Faecalibacterium sp. is Faecalibacterium prausnitzii, (iii) the Akkermansia sp. is Akkermansia muciniphila, (iv) the Myxococcus sp. is Myxococcus xanthus, (v) the Pediococcus sp. is Pediococcus pentosaceus, Pediococcus acidilactici, Pediococcus damnosus, Pediococcus ethanolidurans, or Pediococcus parvulus, the method according to Embodiment 1 or 2.

[0325] Embodiment 4. The method of any one of embodiments 1 to 3, wherein the Myxococcus sp. is in the form of spores, vegetative bacteria, or a mixture of spores and vegetative bacteria.

[0326] Embodiment 5. The method of embodiment 4, wherein the Myxococcus sp. is in the form of a powder containing spores.

[0327] Embodiment 6. The method of any one of embodiments 1-5, wherein the subject is administered fewer than about 20, 15, 10, 9, 8, 7, or 6 different species of bacteria.

[0328] Embodiment 7 The method of embodiment 1, wherein the bacterial population forms part of a bacterial composition.

[0329] Embodiment 8. The method of embodiment 7, wherein the bacterial composition comprises less than about 20, 15, 10, 9, 8, 7, or 6 bacterial species.

[0330] Embodiment 9 The method of embodiment 7 or 8, wherein the bacterial composition is not a fecal transplant.

[0331] Embodiment 10. The method of any one of embodiments 7 to 9, wherein the bacterial composition further comprises a pharmaceutically acceptable excipient.

[0332] Embodiment 11. The method of any one of embodiments 7 to 10, wherein the bacterial composition is a capsule, tablet, suspension, suppository, powder, cream, oil, oil-in-water emulsion, water-in-oil emulsion, or aqueous solution.

[0333] Embodiment 12. The method of any one of embodiments 7 to 10, wherein the bacterial composition is in powder, solid, semi-solid, or liquid form.

[0334] Embodiment 13. The bacterial composition has a water activity (a) at 20°C of less than about 0.9, 0.8, 0.7, 0.6, 0.5, 0.4, 0.3, 0.2, or 0.1. w13. The method of any one of embodiments 7 to 12, wherein

[0335] Embodiment 14. The method of any one of embodiments 7 to 13, wherein the bacterial composition is a food or beverage.

[0336] Embodiment 15. The method of any one of embodiments 7 to 14, wherein the bacterial composition is administered orally or rectally.

[0337] Embodiment 16. The method of any one of embodiments 1 to 15, wherein the Lactobacillus sp., Faecalibacterium sp., Akkermansia sp., Myxococcus sp., and / or Pediococcus sp. is in the form of a powder.

[0338] Embodiment 17. The method of any one of embodiments 1 to 16, wherein the Lactobacillus sp., Faecalibacterium sp., Akkermansia sp., Myxococcus sp., and / or Pediococcus sp. is freeze-dried.

[0339] Embodiment 18. The method of any one of embodiments 1 to 17, wherein the subject is a human.

[0340] Embodiment 19. The method of any one of embodiments 1 to 18, wherein the subject has or lives with someone who has a bacterial, viral, or fungal gastrointestinal infection.

[0341] Embodiment 20. The method of any one of embodiments 1 to 19, wherein the subject has an inflammatory disease.

[0342] Embodiment 21 The method of any one of embodiments 1 to 20, wherein the subject is at risk of suffering from an inflammatory disease.

[0343] Embodiment 22. The method of any one of embodiments 1-21, wherein the subject has at least one, two, three, or four cousins, grandparents, parents, aunts, uncles, and / or siblings who have been diagnosed with an inflammatory disease.

[0344] Embodiment 23. The inflammatory disease is selected from the group consisting of allergy, atopy, asthma, autoimmune disease, autoinflammatory disease, hypersensitivity, childhood allergic asthma, allergic asthma, inflammatory bowel disease, celiac disease, Crohn's disease, colitis, ulcerative colitis, collagenous colitis, lymphocytic colitis, diverticulitis, irritable bowel syndrome, short bowel syndrome, blind loop syndrome, chronic persistent diarrhea, intractable diarrhea of ​​infancy, traveler's diarrhea, immunoproliferative small bowel disease, chronic prostatitis, post-enteritis syndrome, tropical sprue, Whipple's disease, Wolman's disease, arthritis, rheumatoid arthritis, Behcet's disease, uveitis, pyoderma gangrenosum, erythema nodosum, traumatic brain injury, 23. The method of any one of embodiments 20-22, wherein the disease is psoriatic arthritis, juvenile idiopathic arthritis, multiple sclerosis, systemic lupus erythematosus (SLE), myasthenia gravis, juvenile-onset diabetes, type 1 diabetes, Guillain-Barré syndrome, Hashimoto's encephalitis, Hashimoto's thyroiditis, ankylosing spondylitis, psoriasis, Sjogren's syndrome, vasculitis, glomerulonephritis, autoimmune thyroiditis, bullous pemphigoid, sarcoidosis, ichthyosis, Graves' ophthalmopathy, Addison's disease, vitiligo, acne vulgaris, pelvic inflammatory disease, reperfusion injury, sarcoidosis, graft rejection, interstitial cystitis, atherosclerosis, and atopic dermatitis.

[0345] Embodiment 24. The method of embodiment 23, wherein the inflammatory disease is childhood allergic asthma or inflammatory bowel disease.

[0346] Embodiment 25. The method of any one of embodiments 1-24, wherein the subject is suffering from constipation, diarrhea, bloating, urinary urgency, and / or abdominal pain.

[0347] Embodiment 26 The method of any one of embodiments 1 to 25, wherein the subject has received an antibiotic within the last 1, 2, 3, or 4 months.

[0348] Embodiment 27. The method of any one of embodiments 1 to 26, wherein the subject is a newborn.

[0349] Embodiment 28 The method of any one of embodiments 1 to 26, wherein the subject is less than about 1, 2, 3, 4, 5, 6, 7, 8, 9, 12, 18, or 24 months of age.

[0350] Embodiment 29. The method of any one of embodiments 1 to 26, wherein the subject is between about 2 and about 18 years of age, or is at least about 18 years of age.

[0351] Embodiment 30. The subject: (a) Increased rates of Streptococcus spp., Bifidobacterium spp., and Enterococcus spp. compared with the healthy or general population; (b) reduced rates of Alternaria alternata, Aspergillus flavus, Aspergillus cibarius, and Candida sojae compared with the healthy or general population; (c) increased rates of Candida albicans and Debaryomyces spp. compared with the healthy or general population; (d) reduced rates of Bifidobacteria spp., Lactobacillus spp., Faecalibacterium spp., and Akkermansia spp. compared with the healthy or general population; (e) a reduced rate of Malassezia spp. compared with the healthy or general population; (f) an increased proportion of Bacterioides spp., Ruminococcus spp., Prevotella spp., or Bifidobacterium spp. compared with the healthy or general population; or (g) Increased rates of Enterococcus faecalis, Enterococcus faecium, or Clostridium difficile compared with the healthy or general population 30. The method of any one of embodiments 1-29, comprising a gastrointestinal microbiome.

[0352] Embodiment 31. The effective amount is (i) increasing the level of Bifidobacterium sp., Clostridia sp. belonging to clade IV or XIV, Lachnospira sp., and / or Ruminococcus sp. in said subject; (ii) decreasing the pH in the subject's feces; (iii) increasing the level of lactic acid in the subject's feces; (iv) increasing the level of circulating itaconate in said subject; (v) treating, reducing, or preventing allergic inflammation in a subject; (vi) reducing an adaptive immune response in the respiratory tract of said subject; (vii) reducing dendritic cell activation in gastrointestinal-associated mesenteric lymph nodes; (viii) increasing the level of reparative macrophages in the lungs, blood, serum, or plasma of said subject; (ix) increasing the level of an anti-inflammatory compound in said subject; (x) reducing the level of a pro-inflammatory compound in said subject; (xi) reducing the level of eotaxin expression and / or secretion in said subject; and / or reducing the level of mucin expression and / or secretion in said subject 31. The method of any one of embodiments 1 to 30, which is effective for:

[0353] Embodiment 32 The method of embodiment 31, wherein the effective amount is effective to reduce secretion and / or levels of secretion of mucin in the lungs of the subject.

[0354] Embodiment 33 The method of embodiment 31 or 32, wherein the anti-inflammatory compound is a cytokine, a microbial lipid, a microbial carbohydrate, or a microbial amino acid.

[0355] Embodiment 34. The method of embodiment 33, wherein the anti-inflammatory compound is IL-17.

[0356] Embodiment 35. The method of any one of embodiments 31-34, wherein the pro-inflammatory compound is a cytokine, a microbial lipid, a microbial carbohydrate, or a microbial amino acid.

[0357] Embodiment 36. The method of embodiment 35, wherein the pro-inflammatory compound is IL-4, IL-10, IL-8, IL-13, TNF-α, or MUC5B.

[0358] Embodiment 37. The method of one of em...

Claims

1. A composition for use in a method of treating or preventing inflammation or an inflammatory disease in a subject in need thereof, the composition comprising a bacterial population comprising Lactobacillus sp., Faecalibacterium sp., and Ackermansia sp., wherein the Lactobacillus sp. comprises Lactobacillus johnsonii or Lactobacillus crispatus, the Faecalibacterium sp. comprises Faecalibacterium prausnitzii, and the Ackermansia sp. The composition comprises Ackermansia muciniphila, the composition can treat or prevent the inflammation or the inflammatory disease in the subject, and the composition is in a solid or liquid dosage form.

2. A composition for use as described in claim 1, wherein the composition is a solid dosage form.

3. A composition for use as described in claim 1, wherein the composition is in liquid dosage form.

4. The composition for use according to claim 3, wherein the liquid dosage form is formulated for enema administration.

5. The composition for use according to claim 1, wherein the composition is a capsule, tablet, suspension, suppository, powder, cream, oil, emulsion, or aqueous solution or a combination thereof.

6. The composition for use according to claim 5, wherein the composition is a capsule.

7. A composition for use as described in claim 5, wherein the composition is an emulsion.

8. The composition for use according to claim 7, wherein the emulsion is an oil-in-water emulsion, or a water-in-oil emulsion, or a combination thereof.

9. A composition for use as described in claim 5, wherein the composition is a powder or dust.

10. The composition for use according to claim 5, wherein the composition is a suspending agent.

11. A composition for use as described in claim 5, wherein the composition is a tablet.

12. The composition for use according to claim 11, wherein the tablet comprises an inner dosage compartment and an outer dosage compartment.

13. The composition for use according to claim 12, wherein the inner dosage compartment and the outer dosage compartment are separated by an enteric layer.

14. The composition of claim 13, wherein the enteric layer is configured to resist disintegration in the stomach.

15. The composition of claim 13 or 14, wherein the enteric layer is configured to promote delayed release.

16. A composition for use in a method of treating or preventing inflammation or an inflammatory disease in a subject in need thereof, said composition comprising a bacterial population comprising Lactobacillus sp., Faecalibacterium sp., and Ackermansia sp., said Lactobacillus sp. comprising Lactobacillus johnsonii or Lactobacillus crispatus, said Faecalibacterium sp. comprising Faecalibacterium prausnitzii, and said Ackermansia sp. The composition comprises Ackermansia muciniphila, the composition being capable of treating or preventing the inflammation or the inflammatory disease in the subject, the subject being under 90 years of age.

17. The composition for use described in claim 16, wherein the subject is a newborn.

18. The composition for use described in claim 16, wherein the subject is less than 24 months of age.

19. The composition for use according to claim 16, wherein the subject is between 2 and 18 years of age.

20. The composition for use described in claim 16, wherein the subject is at least 18 years of age.

21. The composition for use according to any one of claims 1 to 20, wherein the composition is not a fecal implant.

22. A composition for use according to any one of claims 1 to 21, wherein the bacterial population comprises less than 20 species of bacteria.

23. 23. The composition for use according to any one of claims 1 to 22, wherein the inflammation or inflammatory disease comprises atopy, an autoimmune disease, an autoinflammatory disease, an inflammatory bowel disease, celiac disease, Crohn's disease, colitis, ulcerative colitis, chronic persistent diarrhea, intractable infantile diarrhea, traveller's diarrhea, arthritis, rheumatoid arthritis, psoriatic arthritis, juvenile idiopathic arthritis, multiple sclerosis, systemic lupus erythematosus (SLE), juvenile onset diabetes, type 1 diabetes, psoriasis, pelvic inflammatory disease, transplant rejection, atherosclerosis, or atopic dermatitis.

24. A composition for use according to any one of claims 1 to 23, wherein the composition further comprises a pharma- ceutically acceptable excipient.