Bacterial compositions and methods of treating inflammatory bowel disease

Abstract

Disclosed herein, are compositions comprising Bacteroides uniformis or Blautia sp , and methods of treating gastrointestinal distress, inflammatory bowel disease, as well as preventing weight loss or maintain weight or increasing colon length by administering the compositions to a subject.

Description

[0001] Attorney’s Docket No.: 21101.0478P1 BACTERIAL COMPOSITIONS AND METHODS OF TREATING INFLAMMATORY BOWEL DISEASE CROSS REFERENCE TO RELATED APPLICATIONS This application claims the benefit of priority of U.S. Provisional Application No. 63 / 407,014, filed February 1, 2024 and U.S. Provisional Application No.63 / 639,274, filed April 26, 2024. The content of these earlier filed applications is hereby incorporated by reference herein in their entirety. INCORPORATION OF THE SEQUENCE LISTING The present application contains a sequence listing that is submitted concurrent with the filing of this application, containing the file name “21101_0478P1_SL.xml” which is 12,288 bytes in size, created on January 30, 2025, and is herein incorporated by reference in its entirety. BACKGROUND Currently therapies for inflammatory bowel disease (IBD) include blocking antibodies against important immunological molecules (e.g., IL12, TNF, etc.), however, these therapies often lose efficacy and have side effects that cause loss of efficacy. Microbiota is important in development of IBD and fecal microbiota transplant has limited effectiveness including that there no way to standardize donor fecal material and the potential to transfer harmful organisms. Thus, a need exists to identify specific organisms that are capable of protecting people from this disease. SUMMARY Disclosed herein are compositions comprising Bacteroides uniformis and Blautia sp. Disclosed herein are compositions comprising Bacteroides uniformis or Blautia sp., and a carrier. Disclosed herein are compositions comprising a supernatant from Bacteroides uniformis or Blautia sp. Disclosed herein are compositions comprising a Bacteroides uniformis. Disclosed herein are compositions comprising a Blautia sp. Attorney’s Docket No.: 21101.0478P1 Disclosed herein are methods of treating a subject with gastrointestinal (GI) distress, the methods comprising administering to the subject an effective dose of any of the compositions described herein. In some aspects, the subject has autism spectrum disorder. Disclosed herein are methods of treating inflammatory bowel disease in a subject, the methods comprising administering to the subject an effective dose of any of the compositions described herein, thereby treating inflammatory bowel disease in the subject. In some aspects, the subject has autism spectrum disorder. Disclosed herein are methods of preventing weight loss or maintaining weight in a subject, the methods comprising administering to the subject an effective dose of any of the compositions described herein, thereby preventing weight loss or maintaining weight in the subject. In some aspects, the subject has autism spectrum disorder. Disclosed herein are methods of increasing colon length in a subject, the methods comprising administering to the subject an effective dose of any of the compositions described herein, thereby increasing colon length in the subject. In some aspects, the subject has autism spectrum disorder. BRIEF DESCRIPTION OF THE DRAWINGS The accompanying figures, which are incorporated in and constitute a part of this specification, illustrate several aspects and together with the description serve to explain the principles of the invention. Additional advantages of the invention will be set forth in part in the description which follows, and in part will be obvious from the description, or can be learned by practice of the invention. The advantages of the invention will be realized and attained by means of the elements and combinations particularly pointed out in the appended claims. It is to be understood that both the foregoing general description and the following detailed description are exemplary and explanatory only and are not restrictive of the invention, as claimed. FIGS.1A-E show that repeated DSS injury induces social deficits in mice. FIG.1A shows the percent of original weight of 3-4 week old male mice given DSS (grey) or control mice (black). Background shading illustrates treatment with DSS. FIG.1B shows the area under the curve of the data represented in (FIG.1A), (p=<0.0001). At the end of behavioral testing, day 51, mice were weighed, and euthanized. Colon length (FIG. 1C) was assayed, (p=0.0017). FIGS.3A-C: n=40 animals / treatment analyzed over 4 independent experiments. At day 30 of schedule, mice were analyzed for behavioral changes. FIG.1D show the total movement in the open-field test (n=15 / treatment). FIG.1E show the proportion of total time spent actively socializing with a novel mouse (n=15 / treatment, p=0.0286). Statistics: Attorney’s Docket No.: 21101.0478P1 Bars / lines represent mean values + / - standard error of the mean (SEM). ns p>0.05, * p < 0.05 , ** p < 0.01, *** p < 0.001 for two-tailed unpaired student’s T-test (FIGS.1B-E). FIGS.2A-W show that DSS-induced intestinal phenotypes are worsened by the microbiota from individuals with ASD.6-8 week old male offspring of animals colonized with human microbiotas were subjected to DSS treatment for 7 days (n=4-15). FIG.2A shows the percent of original weight in NT-colonized (black) or ASD-colonized (grey) mice. FIG.2B show AUCs of percent of original weight as shown in (FIG.2A). FIG.2C show colon length at day 7 of DSS injury. FIGS.2D, 2H, 2L, 2P, 2T show pedigrees of 5 families included in the study. Grey shading represents ASD and white represents neuro- typical controls. FIGS. 2E, 2I, 2M, 2Q, 2U show the percent of original weight in NT-colonized (black) or ASD-colonized (grey) mice. FIGS.2F, 2J, 2N, 2R, 2V show AUCs associated with the curves in (FIGS.2E, 2I, 2M, 2Q, 2U). FIGS. 2G, 2K, 2O, 2S, 2W show colon lengths at the end of DSS treatment time course. Statistics: * P < 0.05, ** P < 0.01, *** < P 0.001 for two-tailed unpaired student’s T-test (FIGS. 2B, 2N, 2O), and one- way ANOVA with Tukey’s multiple comparison (FIGS. 2J, 2K, 2S, 2V). FIGS.3A-G show identification of microbes that influence intestinal injury severity. FIG.3A shows PCoA plots of Unweighted Unifrac distances, colored by source. FIG.3B shows PCoA plot of Unweighted Unifrac distances, colored by source and donor. FIG.3C shows PCoA plot of Unweighted Unifrac distances of colonized mice, colored by family: red=family1, blue=2, orange=3, green=4, purple=5. FIG.3D shows Unweighted UniFrac distance values comparing within-donor-neurotype and between-donor-neurotype variation (n = 528-1419). Bars represent mean values ± SEM.FIG.3E shows regression of mean B. uniformis number of reads with mean final percent of original weight in ASD and NT colonized mice. FIG.3F show regression of mean B. uniformis number of reads with endpoint colon length. Coefficient of determination (r2) = 0.6817 and p = 0.0221. FIG. 3G show taxa significantly enriched (by ANCOVA) in either ASD or NT mother in family 3, with Blautia sp. labeled. Statistics: * P < 0.05, *** P < 0.001 for one-way ANOVA with Tukey’s multiple comparison (FIG.3D). FIGS.4A-E show Bacteroides uniformis can reduce DSS severity. FIG.4A shows SPF mice (n=5) were gavaged with B. uniformis or PBS and then subjected to DSS treatment. Squares represent DSS treated mice, circles represent controls. Black represents B. uniformis treated mice, grey represents PBS treated controls. FIG.4A also show the percent of original weight in mice. FIG.4B shows colon length and FIG.4C shows fecal lipocalin (p-0.0711) at the end of DSS treatment. FIG.4D shows representative histology images and FIG.4E shows Attorney’s Docket No.: 21101.0478P1 associated scores from DSS treated mice. Statistics: Bars / lines represent mean values ± SEM. * P < 0.05, ** P < 0.01, *** P < 0.001 for one-way ANOVA with Tukey’s multiple comparison (FIG.4B) and two-tailed unpaired student’s T-test (FIGS.4C.4E). FIGS.5A-I show that Blautia-NT isolated from a NT individual reduces colitis severity. Mice colonized with the microbiota from family 3 (n=3-7) were given DSS and PBS or Blautia-NT supplementation. Circles represent Blautia-treated mice, squares represent controls. Black represents NT-colonized mice, grey represents ASD-colonized mice. FIG.5A shows the percent of original weight loss. FIG.5B shows AUCs associated with (FIG.5A). FIG.5C shows colon length at the end of DSS-colitis. FIG.5D shows histology scores and FIG.5E shows representative images at the end of DSS-colitis. FIGS.5A-D: n=3-6 animals / treatment. FIGS. 5F-I show SPF mice that did or did not receive Blautia-NT treatment before and during acute DSS (7 days of 2.5%). Black circles represents PBS treated mice and gray circles represents Blautia-NT treated mice. FIG.5F show colon length (P=0.0268), FIG.5G shows fecal lipocaline-2 (LCN-2) (p-0.0111), FIG.5H shows histologyscoring (p=0.0006), and FIG. 5I shows representative histological images. FIGS. 5F-I: n=74-week-old animals / treatment. Statistics: Bars / lines represent mean values ± SEM. * P < 0.05,** P < 0.01, *** < P 0.001 for two-way ANOVA with Tukey’s multiple comparison (FIGS. 5B, 5C), two-tailed unpaired student’s T-test (FIG. 5C), and one-way ANOVA with Tukey’s multiple comparison (FIGS. 5F-H). FIGS.6A-B show that Blautia-NT treatment ameliorates intestinal injury-associated defects in social interactions. Mice undergoing a repeated DSS course were treated with either Blautia-NT, B. uniformis or PBS, and subject to three-chamber testing (n =9 or 14 / treatment). FIG.6A shows the ratio of time spent socializing to total time. FIGS. 6B shows the ratio of total active time engaging with novel mouse to time spent in social chamber. Statistics: Bars / lines represent mean values ± SEM. * P < 0.05, ** P < 0.01 for unpaired, two tailed T test. FIGS.7A-K show the behavioral phenotypes not affected by repeated DSS treatment. FIGS.7A-C show mice given repeated DSS were compared for final weight after behavioral analysis. FIG.7A show percent of original weight, FIG.7B shows total weight, and FIG.7C shows fecal lipocalin that were measured. Mice were assayed using an open field test (FIGS. 7D-F. During analysis, the arena was divided into center and peripheral areas. The total time (FIG.7D) entering the center and frequency of times (FIG. 7E) entering the center were analyzed. Mice were assayed using the elevated plus maze and (FIG.7F) assayed for total time on the open arms of the maze, divided by total time tested. FIG.7G shows that the Attorney’s Docket No.: 21101.0478P1 marble burying test was conducted, and the number of marbles buried was assayed. FIGS. 7H-J shows that the tail-suspension test was conducted, and the time spent struggling (FIG. 7H), latency to first stop (FIG.7I), and total time suspended, not struggling (FIG. 7J) was analyzed. FIG.7K shows the time spent within each chamber, during 3-chamber test (n = 15). Statistics: ** P < 0.01 for unpaired, two tailed T test. FIGS.8A-B show the percent of original weight by neurotype. FIG.8A shows a diagram of the experimental design. FIG.8B shows acute DSS colitis, the percent original weight of the mice from an individual microbiota were averaged (displayed as circles, n=6,8). The means of these averages were calculated when grouped by neurotype (plotted as the line). Blue represents ASD-associated microbiotas; red represents NT-associated microbiotas. Statistics: p=0.0627 via repeated measures 2-way ANOVA. FIGS.9A-K show the characterization of microbiotas. FIG.9A shows Unweighted UniFrac distance values, comparing within vs between sample (n = 161, 5378). FIGS.9B-F show Unweighted Unifrac distances when making within-family and between family comparisons (n=66-304). FIG.9G shows ANCOM analysis at the phylum level comparing donor neurotype. FIG.9H shows that Eubacterium sp. reads by donor neurotype. FIG.9I shows regression of Enterobacteriaceae sp. with weight at the end of six days of DSS. FIG. 9J shows regression of Blautia sp. with AUC during acute DSS. Red is NT and blue is ASD. FIG.9K shows Blautia-NT reads in mice, by family and donor. Statistics: * P < 0.05 ** P < 0.01 *** P < 0.001 two-tailed unpaired student’s T-test (FIGS.9A, 9D, 9K) or one-way ANOVA with Tukey’s multiple comparisons (FIGS.9B-F, 9K). FIGS.10A-C show the extended details regarding histology scoring in mice that did or did not receive B. uniformis treatment. FIG. 10A shows crypt loss, FIG.10B show immune cell infiltrate, and FIG.10C shows crypt severity scoring associated with total histology scores. Statistics: ** P < 0.01 two-tailed unpaired student’s T-test. FIGS.11A-C show the extended details regarding histology scoring in mice colonized with either microbiota from family 3, that did or did not receive B. producta–NT treatment. FIG.11A shows crypt loss, FIG.11B shows inflammation, and FIG.11C shows crypt severity scoring associated with total histology scores. Statistics: * P < 0.05, ** P < 0.01 two- tailed unpaired student’s T-test. DETAILED DESCRIPTION The present disclosure can be understood more readily by reference to the following detailed description of the invention, the figures and the examples included herein. Attorney’s Docket No.: 21101.0478P1 Before the present methods and compositions are disclosed and described, it is to be understood that they are not limited to specific synthetic methods unless otherwise specified, or to particular reagents unless otherwise specified, as such may, of course, vary. It is also to be understood that the terminology used herein is for the purpose of describing particular aspects only and is not intended to be limiting. Although any methods and materials similar or equivalent to those described herein can be used in the practice or testing of the present invention, example methods and materials are now described. Moreover, it is to be understood that unless otherwise expressly stated, it is in no way intended that any method set forth herein be construed as requiring that its steps be performed in a specific order. Accordingly, where a method claim does not actually recite an order to be followed by its steps or it is not otherwise specifically stated in the claims or descriptions that the steps are to be limited to a specific order, it is in no way intended that an order be inferred, in any respect. This holds for any possible non-express basis for interpretation, including matters of logic with respect to arrangement of steps or operational flow, plain meaning derived from grammatical organization or punctuation, and the number or type of aspects described in the specification. All publications mentioned herein are incorporated herein by reference to disclose and describe the methods and / or materials in connection with which the publications are cited. The publications discussed herein are provided solely for their disclosure prior to the filing date of the present application. Nothing herein is to be construed as an admission that the present invention is not entitled to antedate such publication by virtue of prior invention. Further, the dates of publication provided herein can be different from the actual publication dates, which can require independent confirmation. DEFINITIONS As used in the specification and the appended claims, the singular forms “a,” “an” and “the” include plural referents unless the context clearly dictates otherwise. The word “or” as used herein means any one member of a particular list and also includes any combination of members of that list. Ranges can be expressed herein as from “about” or “approximately” one particular value, and / or to “about” or “approximately” another particular value. When such a range is expressed, a further aspect includes from the one particular value and / or to the other particular value. Similarly, when values are expressed as approximations, by use of the antecedent “about,” or “approximately,” it will be understood that the particular value forms a further aspect. It will be further understood that the endpoints of each of the ranges are Attorney’s Docket No.: 21101.0478P1 significant both in relation to the other endpoint and independently of the other endpoint. It is also understood that there are a number of values disclosed herein and that each value is also herein disclosed as “about” that particular value in addition to the value itself. For example, if the value “10” is disclosed, then “about 10” is also disclosed. It is also understood that each unit between two particular units is also disclosed. For example, if 10 and 15 are disclosed, then 11, 12, 13, and 14 are also disclosed. As used herein, the terms “optional” or “optionally” mean that the subsequently described event or circumstance may or may not occur and that the description includes instances where said event or circumstance occurs and instances where it does not. As used herein, the term “sample” is meant a tissue or organ from a subject; a cell (either within a subject, taken directly from a subject, or a cell maintained in culture or from a cultured cell line); a cell lysate (or lysate fraction) or cell extract; or a solution containing one or more molecules derived from a cell or cellular material (e.g. a polypeptide or nucleic acid), which is assayed as described herein. A sample may also be any body fluid or excretion (for example, but not limited to, blood, urine, stool, saliva, tears, bile, cerebral spinal fluid) that contains cells or cell components. In some aspects, the sample can be taken from the brain, spinal cord, cerebral spinal fluid or blood. As used herein, the term “subject” refers to the target of administration, e.g., a human. Thus the subject of the disclosed methods can be a vertebrate, such as a mammal, a fish, a bird, a reptile, or an amphibian. The term “subject” also includes domesticated animals (e.g., cats, dogs, etc.), livestock (e.g., cattle, horses, pigs, sheep, goats, etc.), and laboratory animals (e.g., mouse, rabbit, rat, guinea pig, fruit fly, etc.). In one aspect, a subject is a mammal. In another aspect, a subject is a human. The term does not denote a particular age or sex. Thus, adult, child, adolescent and newborn subjects, as well as fetuses, whether male or female, are intended to be covered. As used herein, the term “patient” refers to a subject afflicted with a disease or disorder. The term “patient” includes human and veterinary subjects. In some aspects of the disclosed methods, the “patient” has been diagnosed with a need for treatment for reducing inflammation in the colon or irritable bowel disease, such as, for example, prior to the administering step. In some aspects of the disclosed methods, the “patient” has been diagnosed with a need for treatment for inflammatory bowel disease, such as, for example, prior to the administering step. Attorney’s Docket No.: 21101.0478P1 As used herein, the term “normal” refers to an individual, a sample or a subject that does not have a disease (e.g., an inflammatory bowel disease) or does not have an increased susceptibility of developing a disease (e.g., an inflammatory bowel disease). As used herein, the term “susceptibility” refers to the likelihood of a subject being clinically diagnosed with a disease. For example, a human subject with an increased susceptibility for an inflammatory bowel disease can refer to a human subject with an increased likelihood of a subject being clinically diagnosed with inflammatory bowel disease. As used herein, the term “comprising” can include the aspects “consisting of” and “consisting essentially of.” As used herein, a “control” is a sample from either a normal subject or from tissue from a normal subject that does not have inflammatory bowel disease. As used herein, “over-expression” means expression greater than the expression detected in a normal sample. For example, a nucleic acid that is over-expressed may be expressed about 1 standard deviation above normal, or about 2 standard deviations above normal, or about 3 standard deviations above the normal level of expression. Therefore, a nucleic acid that is expressed about 3 standard deviations above a control level of expression is a nucleic acid that is over-expressed. As used herein, “treat” is meant to mean administer a compound or composition of the invention to a subject, such as a human or other mammal (for example, an animal model), that an inflammatory bowel disease, in order to prevent or delay a worsening of the effects of the disease or condition, or to partially or fully reverse the effects or symptoms of the disease. As used herein, “prevent” is meant to mean minimize the chance that a subject who has an increased susceptibility for developing a disease (e.g., inflammatory bowel disease or will develop inflammatory bowel disease) of actually developing the disease. As used herein, the term “reference,” “reference expression,” “reference sample,” “reference value,” “control,” “control sample” and the like, when used in the context of a sample or expression level of one or more microbes refers to a reference standard wherein the reference is expressed at a constant level among different (i.e., not the same tissue, but multiple tissues) tissues, and is unaffected by the experimental conditions, and is indicative of the level in a sample of a predetermined disease status (e.g., not suffering from an inflammatory bowel disease). The reference value can be a predetermined standard value or a range of predetermined standard values, representing no illness, or a predetermined type or severity of illness. Attorney’s Docket No.: 21101.0478P1 As used herein, the term “probiotic” means microbial cell preparations or components or metabolites of microbial cells with a beneficial effect on the health or well-being of the host (Salminen, S. et al. (1999); Probiotics: how should they be defined, Trends Food Sci. Technol., 10107-10). The definition of probiotic is generally admitted and in line with the WHO definition. The probiotic can comprise a unique strain of microorganism, a mix of various strains and / or a mix of various bacterial species and genera. In case of mixtures, the singular term “probiotic” can still be used to designate the probiotic mixture or preparation. For the purpose of the present invention, spore-forming microbiota or spore-forming bacteria or spore-forming microbes are considered as probiotics. “Prebiotic” generally means a non-digestible food ingredient that beneficially affects the host by selectively stimulating the growth and / or activity of micro-organisms present in the gut of the host, and thus attempts to improve host health (Gibson and Roberfroid “Dietary Modulation of the Human Colonic Microbiota: Introducing the Concept of Prebiotics”, J. Nutr.1995: 125(6):1401-1412). “Prebiotics” alternatively means selectively fermented ingredients that allow specific changes, both in the composition and / or activity in the gastrointestinal microflora, that confer benefits upon the host well-being and health (Roberfroid M. “Prebiotics: the concept revisited”, J. Nutr.2007: 37 (3): 830S-837S). The percentages are by weight unless otherwise stated. The expressions “weight %” and “wt %” are synonymous. They refer to quantities expressed in percent on a dry weight basis. COMPOSITIONS Disclosed herein are compositions comprising a Bacteroides uniformis or a Blautia sp, and a carrier. Further disclosed herein are compositions comprising Bacteroides uniformis or Blautia sp., or a combination thereof, and a carrier. In some aspects, the Blautia sp. can be identified by its 16S ribosomal gene sequence. In some aspects, the Blautia sp. hasa 16S ribosomal gene sequence having the sequence set forth in SEQ ID NO: 1 or SEQ IDNO: 2. In some aspects, the Blautia sp. comprises a 16S rRNA sequence that is at least about 95%, or at least about 97%, or at least about 98%, or at least about 99% sequence identity with nucleotide sequences selected from SEQ ID NO: 1 and SEQ ID NO: 2. In some aspects, the Bacteroides uniformis can be identified by its 16S ribosomal gene sequence. Blautia sp. Disclosed herein is a bacteria, Blautia sp. Blautia sp. as used herein refers to a bacteria having a 16S nucleic acid sequence sharing at least 98% sequence identity to SEQ ID NO: 1. In some aspects, the genome assembly of the Blautia sp. has NRRL or ATCC Attorney’s Docket No.: 21101.0478P1 Accession number PRJNA952791. In some aspects, Blautia sp. was isolated from a stool from a healthy human subject. Blautia sp. Disclosed herein is a bacteria, Blautia sp. Blautia sp. as used herein refers to a bacteria having a 16S nucleic acid sequence sharing at least 98% sequence identity to SEQ ID NO: 2. In some aspects, the genome assembly of the Blautia sp. has NRRL or ATCC Accession number PRJNA952791. In some aspects, the Blautia sp. was isolated from a stool from a healthy human subject. Bacteroides uniformis. Disclosed herein is a bacteria, B. uniformis. In some aspects, the B. uniformis has NRRL or ATCC Accession number 8492. In some aspects, the genome of B. uniformis strain ATCC 8492 has Bioproject number PRJNA18195 In some aspects, the B. uniformis was isolated from a human stool. Disclosed herein are compositions comprising a Bacteroides uniformis and a carrier. Disclosed herein are compositions comprising a Blautia sp. and a carrier. Disclosed herein are compositions comprising a Bacteroides uniformis and a Blautia sp. and a carrier. Disclosed herein are compositions consisting of a Bacteroides uniformis and a carrier. Disclosed herein are compositions consisting of a Blautia sp. and a carrier. Disclosed herein are compositions consisting of a Bacteroides uniformis and a Blautia sp. and a carrier. Disclosed herein are a Bacteroides uniformis and / or a Blautia sp. for treating a subject with gastrointestinal distress, treating a subject with inflammatory bowel disease, and preventing weight loss or maintain weight in a subject. In some aspects, the Bacteroides uniformis and / or Blautia sp. can be identified by their 16S ribosomal gene sequence. In some aspects, the Blautia sp. has a 16S ribosomal gene sequence having thesequence set forth in SEQ ID NO: 1 or SEQ ID NO: 2. In some aspects, the Blautia sp.comprises a 16S rRNA sequence that is at least about 95%, or at least about 97%, or at least about 98%, or at least about 99% sequence identity with nucleotide sequences selected from SEQ ID NO: 1 and SEQ ID NO: 2. In some aspects, the Bacteroides uniformis can be identified by its 16S ribosomal gene sequence. Table 1. Name Sequence SEQ D O: Attorney’s Docket No.: 21101.0478P1 Blautia sp., TCAGAGAGTTTGATCCTGGCTCAGGATGAACGCTGGCGGCGTGCT 1 (16s TAACACATGCAAGTCGAGCGAAGCACTTAAGTGGATCTCTTCGGA Attorney’s Docket No.: 21101.0478P1 CGATAACTGGGGTGAAGTCGTAACAAGGTAGCCGTATCGGAAGG TGCGGCTGGATCACCTCCTTT Attorney’s Docket No.: 21101.0478P1 TGTACACACCGCCCGTCACACCATGGGAGTCAGTAACGCCCGAA GTCAGTGACCCAACCTTTTAGGAGGGAGCTGCCGAAGGCGGGAC uniformis. Disclosed herein are compositions comprising a supernatant from a Blautia sp. Disclosed herein are compositions comprising a supernatant from a Bacteroides uniformis and a Blautia sp. Disclosed herein are compositions comprising: one or more isolated microbial organisms or a component of the isolated microbial organism, wherein the one or more isolated microbial organisms comprise Bacteroides uniformis and Blautia sp., a mixture thereof, or a component derived therefrom, wherein the composition is formulated as a supplement, a powder, a pill, a tablet, a capsule, a pharmaceutical composition, a nutraceutical composition, or a probiotic composition. In some aspects, the isolated microbial organism is cultured bacteria. In some aspects, the isolated microbial organism comprise bacterial outer membrane vesicles derived from the isolated microbial organism. In some aspects, the Blautia sp. has a 16S ribosomal gene sequence having the sequence set forth in SEQ ID NO: 1 or SEQ ID NO: 2. In some aspects, the Blautia sp. comprises a 16S rRNA sequence that is at least about 95%, or at least about 97%, or at least about 98%, or at least about 99% sequence identity with nucleotide sequences selected from SEQ ID NO: 1 and SEQ ID NO: 2. In some aspects, the Bacteroides uniformis can be identified by its 16S ribosomal gene sequence. Also disclosed are pharmaceutical compositions comprising a plurality of bacterial isolates, wherein the plurality of bacterial isolates comprise one or more isolated microbial organisms or a component of the isolated microbial organism, wherein the one or more isolated microbial organisms comprise Bacteroides uniformis and Blautia sp., a mixture thereof.. In some aspects, the isolated microbial organism is cultured bacteria. In some aspects, the isolated microbial organism comprise bacterial outer membrane vesicles derived from the isolated microbial organism. In some aspects, the Blautia sp. has a 16S ribosomalgene sequence having the sequence set forth in SEQ ID NO: 1 or SEQ ID NO: 2. In someaspects, the Blautia sp. comprises a 16S rRNA sequence that is at least about 95%, or at least about 97%, or at least about 98%, or at least about 99% sequence identity with nucleotide Attorney’s Docket No.: 21101.0478P1 sequences selected from SEQ ID NO: 1 and SEQ ID NO: 2.In some aspects, the Bacteroides uniformis can be identified by its 16S ribosomal gene sequence. In some aspects, any of the compositions disclosed herein are capable of preventing weight loss or maintaining weight in a subject. In some aspects, any of the compositions disclosed herein are capable of increasing colon length in a subject. In some aspects, the compositions disclosed herein are capable of replacing microbiota of a subject with a disease or disorder associated with an imbalanced microbiota. In some aspects, the compositions disclosed herein are capable of replacing microbiota of a subject with a disease or disorder associated with a dysfunctional microbiota. In some aspects, the compositions disclosed herein are capable of replacing microbiota of a subject with a disease or disorder associated with microbiota that is decreased in functional diversity. In some aspects, the compositions disclosed herein are capable of replacing microbiota of a subject with a disease or disorder associated with an imbalanced microbiota. In some aspects, the imbalanced microbiota can be a decrease in Bacteroides uniformis. In some aspects, the imbalanced microbiota can be a decrease in Blautia sp. In some aspects, the imbalanced microbiota can be a decrease in Bacteroides uniformis and a decrease of Blautia sp. In some aspects, the disease or disorder can be an inflammatory bowel disease. In some aspects, the inflammatory bowel disease can be Crohn’s disease or ulcerative colitis. In some aspects, the disclosed compositions can comprise a bacterial microorganism identifiable by homology of at least 95, 96, 97, 98, 99, or greater percent identity to the 16S ribosomal sequences of SEQ ID NO: 1 or SEQ ID NO: 2. In some aspects, the amount of 16S sequence is less than about 1.2 kb, 1.1 kb, 1.0 kb, 0.9 kb, 8 kb, 0.7 kb, 0.6 kb, 0.5 kb, 0.4 kb, 0.3 kb, 0.2 kb, or 0.1 kb and greater than about 50 nt, 0.1 kb, 2 kb, 0.3 kb, 0.4 kb, 0.5 kb, 0.6 kb, 0.7 kb, 0.8 kb, 0.9 kb, 1.0 kb, or 1.1 kb. In some aspects, the amount of 16S ribosomal sequence homology is between about 150 nt and 500 nt, for example about 250 nt. To determine the percent identity of two nucleic acids, the sequences are aligned for optimal comparison purposes (e.g., gaps can be introduced in the sequence of a first nucleic acid sequence for optimal alignment with a second nucleic acid sequence). The nucleotides at corresponding nucleotide positions are then compared. When a position in the first sequence is occupied by the same nucleotide as the corresponding position in the second sequence, then the molecules are identical at that position. The percent identity between the two Attorney’s Docket No.: 21101.0478P1 sequences is a function of the number of identical positions shared by the sequences (i.e., % identity = # of identical positions / total # of positions times 100). The determination of percent homology between two sequences can be accomplished using a mathematical algorithm. A preferred, non-limiting example of a mathematical algorithm utilized for the comparison of two sequences is the algorithm of Karlin and Altschul (1990) Proc. Nat'l Acad. Sci. USA 87:2264-2268, modified as in Karlin and Altschul (1993) Proc. Nat'l Acad. Sci. USA 90:5873-5877. Such an algorithm is incorporated into the NBLAST and XBLAST programs of Altschul, et al. (1990) J. Mol. Biol.215:403- 410. BLAST nucleotide searches can be performed with the NBLAST program, score=100, word length=12 to obtain nucleotide sequences similar or homologous to nucleic acid molecules of the present disclosure. To obtain gapped alignments for comparison purposes, Gapped BLAST can be utilized as described in Altschul et al. (1997) Nucleic Acids Res. 25:3389-3402. When utilizing BLAST and Gapped BLAST programs, the default parameters of the respective programs (e.g., XBLAST and NBLAST) can be used. These algorithms may be used to align DNA with RNA, and in some cases may be used to align proteins with translated nucleotide sequences. In some aspects, at least two or more microorganisms are included in the compositions of the present disclosure. It is contemplated that where two or more microorganisms form the composition, the microorganisms may be co-cultured to produce the disclosed composition. In some aspects, the disclosed composition can be formed by combining individual cultures of the two or more strains. The microorganisms can be propagated by methods known in the art. For example, the microorganisms can be propagated in a liquid medium under anaerobic or aerobic conditions. Suitable liquid mediums used for growing microorganism include those known in the art such as Nutrient Broth and Tryptic soy agar (TSA), etc. In some aspects, the composition includes the entire listing of the strains listed in Table 1. In some aspects, the composition includes at least two or more of the following strains: Bacteroides uniformis and Blautia sp. In some aspects, the compositions disclosed herein can comprise at least 1x104cells of each bacterial strain. In some aspects, the compositions disclosed herein can comprise at least 1x105cells of each bacterial strain. In some aspects, the compositions disclosed herein can comprise at least 1x106cells of each bacterial strain. In some aspects, the compositions disclosed herein can comprise at least 1x107cells of each bacterial strain. In some aspects, the compositions disclosed herein can comprise at least 1x108cells of each bacterial strain. In some aspects, the compositions disclosed herein can comprise at least 1x109cells of each Attorney’s Docket No.: 21101.0478P1 bacterial strain. In some aspects, the compositions disclosed herein can comprise at least 1x1010cells of each bacterial strain. In some aspects, a single dosage of any of the compositions disclosed herein can comprise between 1x104and 1x1010cells of each bacterial strain. In some aspects, the cells of the consortia are active. In some aspects, the compositions disclosed herein can further comprising a pharmaceutically acceptable carrier. In some aspects, the compositions can also include additives. Suitable additives include substances known in the art that may support growth, production of specific metabolites by the microorganism, alter pH, enrich for target metabolites, enhance insecticidal effects, and combinations thereof. Exemplary additives include carbon sources, nitrogen sources, phosphorous sources, inorganic salt, organic acid, growth media, vitamins, minerals, acetic acid, amino acids and the like. Examples of suitable carbon sources include, without limitation, starch, peptone, yeast extract, amino acids, sugars such as sucrose, glucose, arabinose, mannose, glucosamine, maltose, sugar cane, alfalfa extracts, molasses, rum, and the like; salts of organic acids such as acetic acid, fumaric acid, adipic acid, propionic acid, citric acid, gluconic acid, malic acid, pyruvic acid, malonic acid, isovaleric acid, valeric acid, butyric acid and the like; alcohols such as ethanol, glycerol, and the like; oil or fat such as soybean oil, rice bran oil, olive oil, corn oil, and sesame oil. The amount of the carbon source added varies according to the kind of carbon source and is typically between 1 to 100 grams per liter of medium. The weight fraction of the carbon source in the composition may be about 98% or less, about 95% or less, about 90% or less, about 85% or less, about 80% or less, about 75% or less, about 70% or less, about 65% or less, about 60% or less, about 55% or less, about 50% or less, about 45% or less, about 40% or less, about 35% or less, about 30% or less, about 25% or less, about 20% or less, about 15% or less, about 10% or less, about 5% or less, about 2%, or about 1% or less of the total weight of the composition. Preferably, alfalfa is contained in the medium as a major carbon source, at a concentration of about 1 to 20% (w / v). More preferably, the alfalfa is at a concentration of about 5 to 12% (w / v). Examples of suitable nitrogen sources include, without limitation, amino acids, yeast extract, alfalfa extract, tryptone, beef extract, peptone, potassium nitrate, ammonium nitrate, ammonium chloride, ammonium sulfate, ammonium phosphate, ammonia or combinations thereof. The amount of nitrogen source varies according to the nitrogen source, typically between 0.1 to 30 grams per liter of medium. The weight fraction of the nitrogen source in the composition may be about 98% or less, about 95% or less, about 90% or less, about 85% or less, about 80% or less, about 75% or less, about 70% or less, about 65% or less, about Attorney’s Docket No.: 21101.0478P1 60% or less, about 55% or less, about 50% or less, about 45% or less, about 40% or less, about 35% or less, about 30% or less, about 25% or less, about 20% or less, about 15% or less, about 10% or less, about 5% or less, about 2%, or about 1% or less of the total weight of the composition. Examples of suitable inorganic salts include, without limitation, potassium dihydrogen phosphate, dipotassium hydrogen phosphate, disodium hydrogen phosphate, magnesium sulfate, magnesium chloride, ferric sulfate, ferrous sulfate, ferric chloride, ferrous chloride, manganous sulfate, manganous chloride, zinc sulfate, zinc chloride, cupric sulfate, calcium chloride, sodium chloride, calcium carbonate, sodium carbonate, and combinations thereof. The weight fraction of the inorganic salt in the composition may be about 98% or less, about 95% or less, about 90% or less, about 85% or less, about 80% or less, about 75% or less, about 70% or less, about 65% or less, about 60% or less, about 55% or less, about 50% or less, about 45% or less, about 40% or less, about 35% or less, about 30% or less, about 25% or less, about 20% or less, about 15% or less, about 10% or less, about 5% or less, about 2%, or about 1% or less of the total weight of the composition. In some aspects, the compositions of the present disclosure can further comprise acetic acid or carboxylic acid. Suitable acetic acids include any known in the art including, without limitation, formic acid, acetic acid, propionic acid, butanoic acid, isobutyric acid, 3- methyl butanoic acid, methyl acetate ethyl acetate, propyl acetate, butyl acetate, isobutyl acetate, isovaleric acid, valeric acid, butyric acid, and 2-methyl butyl acetate. In some aspects, the acetic acid is included by using vinegar. The weight fraction of the acetic acid in the composition may be about 98% or less, about 95% or less, about 90% or less, about 85% or less, about 80% or less, about 75% or less, about 70% or less, about 65% or less, about 60% or less, about 55% or less, about 50% or less, about 45% or less, about 40% or less, about 35% or less, about 30% or less, about 25% or less, about 20% or less, about 15% or less, about 10% or less, about 5% or less, about 2%, or about 1% or less of the total weight of the composition. In some aspects, the compositions disclosed herein can be frozen. In some aspects, the bacteria can be frozen in 25% anaerobically reduced PBS+ 0.1% L-Cystine or 5% DMSO. The compositions of the present disclosure can be in liquid or dry form. In some aspects, the compositions disclosed herein can be a solid. In some aspects, the compositions disclosed herein can be a liquid. In some aspects, the composition can comprise an aqueous suspension of components. This aqueous suspension can be provided as a concentrated stock solution which is diluted prior to application or as a diluted solution ready-to-use. Also, the Attorney’s Docket No.: 21101.0478P1 composition can be a powder, granules, dust, pellet or colloidal concentrate. Such dry forms may be formulated to dissolve immediately upon wetting or dissolve in a controlled-release, sustained-release, or other time-dependent manner. Also, the composition may be in a dry form that does not depend upon wetting or dissolving to be effective. In some aspects, the composition of the present disclosure can comprise at least one optional excipient. Non-limiting examples of suitable excipients include antioxidants, additives, diluents, binders, fillers, buffering agents, mineral salts, pH modifying agents, disintegrants, dispersing agents, flavoring agents, nutritive agents, oncotic and osmotic agents, stabilizers, preservatives, palatability enhancers and coloring agents. The amount and types of excipients utilized to form the combination may be selected according to known principles of science. In some aspects, the excipient can include at least one diluent. Non-limiting examples of suitable diluents include microcrystalline cellulose (MCC), cellulose derivatives, cellulose powder, cellulose esters (i.e., acetate and butyrate mixed esters), ethyl cellulose, methyl cellulose, hydroxypropyl cellulose, hydroxypropyl methylcellulose, sodium carboxymethylcellulose, corn starch, phosphated corn starch, pregelatinized corn starch, rice starch, potato starch, tapioca starch, starch-lactose, starch-calcium carbonate, sodium starch glycolate, glucose, fructose, lactose, lactose monohydrate, sucrose, xylose, lacitol, mannitol, malitol, sorbitol, xylitol, maltodextrin, and trehalose. In some aspects, the excipient can comprise a binder. Suitable binders include, but are not limited to, starches, pregelatinized starches, gelatin, polyvinylpyrrolidone, cellulose, methylcellulose, sodium carboxymethylcellulose, ethylcellulose, polyacrylamides, polyvinyloxoazolidone, polyvinylalcohols, C12-C18 fatty acid alcohol, polyethylene glycol, polyols, saccharides, oligosaccharides, polypeptides, oligopeptides, and combinations thereof. In some aspects, the excipient can include a filler. Suitable fillers include, but are not limited to, carbohydrates, inorganic compounds, and polyvinylpyrrolidone. By way of non- limiting example, the filler may be calcium sulfate, both di- and tri-basic, starch, calcium carbonate, magnesium carbonate, microcrystalline cellulose, dibasic calcium phosphate, magnesium carbonate, magnesium oxide, calcium silicate, talc, modified starches, lactose, sucrose, mannitol, or sorbitol. In some aspects, the excipient can comprise a buffering agent. Representative examples of suitable buffering agents include, but are not limited to, MOPS, HEPES, TAPS, Attorney’s Docket No.: 21101.0478P1 Bicine, Tricine, TES, PIPES, MES, Tris buffers or buffered saline salts (e.g., Tris buffered saline or phosphate buffered saline). In some aspects, the excipient can include a disintegrant. Suitable disintegrants include, but are not limited to, starches such as cornstarch, potato starch, pregelatinized and modified starches thereof, sweeteners, clays, such as bentonite, microcrystalline cellulose, alginates, sodium starch glycolate, gums such as agar, guar, locust bean, karaya, pecitin, and tragacanth. In some aspects, the excipient can include a dispersion enhancer. Suitable dispersants may include, but are not limited to, starch, alginic acid, polyvinylpyrrolidones, guar gum, kaolin, bentonite, purified wood cellulose, sodium starch glycolate, isoamorphous silicate, and microcrystalline cellulose. In some aspects, the excipient can include a lubricant. Non-limiting examples of suitable lubricants include minerals such as talc or silica; and fats such as vegetable stearin, magnesium stearate or stearic acid. The weight fraction of the excipient(s) in the combination can be about 98% or less, about 95% or less, about 90% or less, about 85% or less, about 80% or less, about 75% or less, about 70% or less, about 65% or less, about 60% or less, about 55% or less, about 50% or less, about 45% or less, about 40% or less, about 35% or less, about 30% or less, about 25% or less, about 20% or less, about 15% or less, about 10% or less, about 5% or less, about 2%, or about 1% or less of the total weight of the combination. In some aspects, the compositions of the present disclosure are stable at room temperature. In some aspects, the consortia or compositions disclosed herein can be kept at a reduced temperature for storage and transportation without significantly compromising the viability of the live bacterial microorganisms. The consortia or compositions comprising the same can be refrigerated, frozen, or lyophilized. The compositions may be refrigerated at between 32°F to 44°F. In some aspects, the consortia or compositions comprising the same can be stored and transported in a frozen state. The live beneficial bacterial microorganisms can be reinvigorated quickly once the compositions are thawed and brought to ambient temperature, for example, with aeration and / or agitation. In some aspects, the compositions can be stored and transported in a manner that limits their exposure to oxygen. In some aspects, live beneficial bacterial microorganisms can be reinvigorated quickly once the compositions are thawed and brought to ambient Attorney’s Docket No.: 21101.0478P1 temperature, for example, with aeration and / or agitation in an anaerobic environment. In some aspects, live beneficial bacterial microorganisms can be reinvigorated quickly once the compositions are thawed and brought to ambient temperature, for example, with aeration and / or agitation in an aerobic environment. In some aspects, the compositions and / or bacterial strains can be lyophilized. The compositions and / or bacterial strains can be first frozen. Water can be then removed amendments under vacuum. This process further reduces the weight of the composition for storage and transportation. The compositions and / or bacterial strains can be reconstituted and reinvigorated prior to application or administration. In some aspects, the compositions can be diluted with water before application or administration. Diluted compositions can be stored for a prolonged period of time, e.g., as long as 30 days, without losing viability. To maintain the live beneficial bacterial microorganism in a substantially aerobic state, dissolved oxygen in the diluted compositions of the present disclosure are preferably kept at an optimal level. It is preferable to supply optimal amounts of oxygen to the diluted composition though slow aeration. In some aspects, any of the composition disclosed herein can be administered in a form selected from the group consisting of powder, granules, a ready-to-use beverage, food bar, an extruded form, capsules, gel caps, and dispersible tablets. Deposit information. A deposit of bacterium Blautia sp., which is disclosed herein, was made with the American Type Culture Collection (ATCC), 10801 University Blvd., Manassas, VA 20110-2209. The date of deposit is ______ and the accession number for the deposited bacterium Blautia sp. is ATCC Accession No. ----------. All restrictions upon the deposit have been removed, and the deposit is intended to meet all of the requirements of 37 C.F.R. §1.801-1.809. The deposit will be maintained in the depository for a period of 30 years, or 5 years after the last request, or for the effective life of the patent, whichever is longer, and will be replaced if necessary during that period. METHODSDisclosed herein are methods of treating a subject with inflammatory bowel disease. In some aspects, the methods can comprise administering to the subject any of the compositions disclosed herein. In some aspects, disclosed are methods of treating a subject with inflammatory bowel disease comprising administering to the subject a composition comprising: one or more isolated microbial organisms or a component of the isolated microbial organism, wherein the one or more isolated microbial organisms comprise Bacteroides uniformis and Blautia sp., a mixture thereof, or a component derived therefrom. Attorney’s Docket No.: 21101.0478P1 In some aspects, the composition is formulated as a supplement, a powder, a pill, a tablet, a capsule, a pharmaceutical composition, a nutraceutical composition, or a probiotic composition. In some aspects, the isolated microbial organism is cultured bacteria. In some aspects, the isolated microbial organism comprise bacterial outer membrane vesicles derived from the isolated microbial organism. In some aspects, the Blautia sp. has a 16S ribosomalgene sequence having the sequence set forth in SEQ ID NO: 1 or SEQ ID NO: 2. In someaspects, the Blautia sp. comprises a 16S rRNA sequence that is at least about 95%, or at least about 97%, or at least about 98%, or at least about 99% sequence identity with nucleotide sequences selected from SEQ ID NO: 1 and SEQ ID NO: 2. In some aspects, the Bacteroides uniformis can be identified by its 16S ribosomal gene sequence. In some aspects, the subject has autism spectrum disorder. Disclosed herein are methods of treating a subject with GI distress. In some aspects, the methods can comprise administering to the subject any of the compositions disclosed herein. In some aspects, disclosed are methods of treating a subject with GI distress comprising administering to the subject a composition comprising: one or more isolated microbial organisms or a component of the isolated microbial organism, wherein the one or more isolated microbial organisms comprise Bacteroides uniformis and Blautia sp., a mixture thereof, or a component derived therefrom. In some aspects, the composition is formulated as a supplement, a powder, a pill, a tablet, a capsule, a pharmaceutical composition, a nutraceutical composition, or a probiotic composition. In some aspects, the isolated microbial organism is cultured bacteria. In some aspects, the isolated microbial organism comprise bacterial outer membrane vesicles derived from the isolated microbial organism. In some aspects, the Blautia sp. has a 16S ribosomal gene sequence having the sequence set forth in SEQ ID NO: 1 or SEQ ID NO: 2. In some aspects, the Blautia sp. comprises a 16S rRNA sequence that is at least about 95%, or at least about 97%, or at least about 98%, or at least about 99% sequence identity with nucleotide sequences selected from SEQ ID NO: 1 and SEQ ID NO: 2. In some aspects, the Bacteroides uniformis can be identified by its 16S ribosomal gene sequence. In some aspects, the subject has autism spectrum disorder. Disclosed herein are methods of preventing weight loss or maintaining weight in a subject. In some aspects, the methods can comprise administering to the subject any of the compositions disclosed herein. In some aspects, disclosed are methods of preventing weight loss or maintaining weight in a subject comprising administering to the subject a composition comprising: one or more isolated microbial organisms or a component of the isolated microbial organism, wherein the one or more isolated microbial organisms comprise Attorney’s Docket No.: 21101.0478P1 Bacteroides uniformis and Blautia sp., a mixture thereof, or a component derived therefrom. In some aspects, the composition is formulated as a supplement, a powder, a pill, a tablet, a capsule, a pharmaceutical composition, a nutraceutical composition, or a probiotic composition. In some aspects, the isolated microbial organism is cultured bacteria. In some aspects, the isolated microbial organism comprise bacterial outer membrane vesicles derived from the isolated microbial organism. In some aspects, the Blautia sp. has a 16S ribosomalgene sequence having the sequence set forth in SEQ ID NO: 1 or SEQ ID NO: 2. In someaspects, the Blautia sp. comprises a 16S rRNA sequence that is at least about 95%, or at least about 97%, or at least about 98%, or at least about 99% sequence identity with nucleotide sequences selected from SEQ ID NO: 1 and SEQ ID NO: 2. In some aspects, the Bacteroides uniformis can be identified by its 16S ribosomal gene sequence. In some aspects, the subject has autism spectrum disorder. Disclosed herein are methods of increasing colon length in a subject. In some aspects, the methods can comprise administering to the subject any of the compositions disclosed herein. In some aspects, disclosed are methods of increasing colon length in a subject comprising administering to the subject a composition comprising: one or more isolated microbial organisms or a component of the isolated microbial organism, wherein the one or more isolated microbial organisms comprise Bacteroides uniformis and Blautia sp., a mixture thereof, or a component derived therefrom. In some aspects, the composition is formulated as a supplement, a powder, a pill, a tablet, a capsule, a pharmaceutical composition, a nutraceutical composition, or a probiotic composition. In some aspects, the isolated microbial organism is cultured bacteria. In some aspects, the isolated microbial organism comprise bacterial outer membrane vesicles derived from the isolated microbial organism. In some aspects, the Blautia sp. has a 16S ribosomal gene sequence having the sequence set forth in SEQ ID NO: 1 or SEQ ID NO: 2. In some aspects, the Blautia sp. comprises a 16S rRNA sequence that is at least about 95%, or at least about 97%, or at least about 98%, or at least about 99% sequence identity with nucleotide sequences selected from SEQ ID NO: 1 and SEQ ID NO: 2. In some aspects, the Bacteroides uniformis can be identified by its 16S ribosomal gene sequence. In some aspects, the subject has autism spectrum disorder. In some aspects of the methods disclosed herein, the subject has autism spectrum disorder. Disclosed herein are methods of altering relative abundance of microbiota in a subject. In some aspects, disclosed are methods of altering relative abundance of microbiota in a subject comprising administering to the subject a composition comprising: one or more Attorney’s Docket No.: 21101.0478P1 isolated microbial organisms or a component of the isolated microbial organism, wherein the one or more isolated microbial organisms comprise Bacteroides uniformis and Blautia sp., a mixture thereof, or a component derived therefrom. In some aspects, the composition is formulated as a supplement, a powder, a pill, a tablet, a capsule, a pharmaceutical composition, a nutraceutical composition, or a probiotic composition. In some aspects, the isolated microbial organism is cultured bacteria. In some aspects, the isolated microbial organism comprise bacterial outer membrane vesicles derived from the isolated microbial organism. In some aspects, the Blautia sp. has a 16S ribosomal gene sequence having thesequence set forth in SEQ ID NO: 1 or SEQ ID NO: 2. In some aspects, the Blautia sp.comprises a 16S rRNA sequence that is at least about 95%, or at least about 97%, or at least about 98%, or at least about 99% sequence identity with nucleotide sequences selected from SEQ ID NO: 1 and SEQ ID NO: 2.In some aspects, the Bacteroides uniformis can be identified by its 16S ribosomal gene sequence. In some aspects, the subject has autism spectrum disorder. In some aspects, the methods can comprise administering to the subject an effective dose of any of the compositions disclosed herein, thereby altering the relative abundance of microbiota in the subject. In some aspects, the methods can comprise administering to the subject an effective dose of a composition comprising Bacteroides uniformis and / or Blautia sp., thereby altering the relative abundance of microbiota in the subject. In some aspects, the methods can comprise administering to the subject an effective dose of a composition comprising at least Blautia sp. having a 16S rDNA sequence comprising SEQ ID NO: 1 or SEQ ID NO: 2, thereby altering the relative abundance of microbiota in the subject. In some aspects, the relative abundance of Bacteroides uniformis can be increased. In some aspects, the relative abundance of Blautia sp. can be increased. In some aspects, the relative abundance of Bacteroides uniformis and Blautia sp. can be increased. In some aspects, the relative abundance of Bacteroides uniformis can be replaced. In some aspects, the relative abundance of Blautia sp. can be replaced. In some aspects, the relative abundance of Bacteroides uniformis and Blautia sp. can be replaced. In some aspects, the compositions disclosed herein can be for replacing microbiota of a subject with a disease or disorder associated with an imbalanced microbiota (or dysfunctional microbiota or a microbiota that is decreased in functional diversity). The method of altering microbiota can also include measuring the relative abundance of one or more microbiota in a sample from a subject. As used herein, the term “relative abundance” refers to the commonality or rarity of an organism relative to other organisms in a defined location or community. For example, the relative abundance can be determined by Attorney’s Docket No.: 21101.0478P1 generally measuring the presence of a particular organism compared to the total presence of organisms in a sample. The relative abundance of microbiota can be measured directly or indirectly. Direct measurements can include culture-based methods. Indirect measurements can include comparing the prevalence of a molecular indicator of identity, such as ribosomal RNA (rRNA) gene sequences, specific for an organism or group of organisms in relation to the overall sample. For example, a ratio of rRNA specific for Bacteroides uniformis in a total number of rRNA gene sequences obtained from a cecal sample can be used to determine the relative abundance of Bacteroides uniformis in the cecal sample. As used herein, the term “microbiota” is used to refer to one or more bacterial communities that can be found or can exist (colonize) within a gastrointestinal tract of an organism. When referring to more than one microbiota, the microbiota can be of the same type (strain) or it can be a mixture of taxa. In some aspects, the methods and compositions disclosed herein that alter the relative abundance of microbiota from genera such as Bacteroides and / or Blautia in a gastrointestinal tract of a subject. The relative abundance microbiota can be altered by administering a pharmaceutical composition that includes microbiota from genera such as Bacteroides and / or Blautia or a compound that substantially increases the relative abundance of microbiota from genera such as Bacteroides and / or Blautia. In some aspects, the relative abundance of Bacteroides and / or Blautia can be increased in the subject by at least about 5%. In some aspects, the relative abundance of Bacteroides and / or Blautia can be increased in the subject by at least about 10%. In some aspects, the relative abundance of Bacteroides and / or Blautia can be increased in the subject by at least about 1%, 2%, 3%, 4%, 5%, 6%, 7%, 8%, 9%, or 10%. In some aspects, the relative abundance of at least one of species of Bacteroides and / or Blautia can be increased by 5%. In some aspects, the methods disclosed herein can further comprise administering a second therapeutic agent to the subject. In some aspects, the second therapeutic agent can be one or more bacteriophages. In some aspects, the second therapeutic agent can be one or more commercially available therapeutic agents that can be administered to treat inflammatory bowel disease. In some aspects, the second therapeutic agent can be an anti- inflammatory agent. In some aspects, in any of the methods disclosed herein, the subject has been identified as being in need of the treatment. In some aspects, the subject has inflammatory Attorney’s Docket No.: 21101.0478P1 bowel disease. In some aspects, the inflammatory bowel disease can be Crohn’s disease or ulcerative colitis. In some aspects, the subject has autism spectrum disorder. In some aspects, the subject has autism spectrum disorder and an inflammatory bowel disease. In some aspects, the subject has gastrointestinal distress. In some aspects, the subject has autism and gastrointestinal distress. In some aspects, gastrointestinal distress can include any digestive disorder that is associated with lingering symptoms of constipation, bloating, reflux, nausea, vomiting, diarrhea, abdominal pain, inflammation, cramping, or a combination thereof. In some aspects, the step of administering any of the compositions disclosed herein can comprise delivering the composition to at least a stomach, a small intestine, or a large intestine of the subject. In some aspects, the composition can be administered orally. In some aspects, the subject can be a human. In some aspects, the cells of the composition are active. In some aspects, the cells of the bacterial strains disclosed herein are active. Disclosed herein are methods of treating a subject with gastrointestinal distress. In some aspects, the methods can comprise administering to the subject any of the compositions disclosed herein, wherein the relative abundance of Bacteroides uniformis and / or Blautia sp. is increased in the subject compared to the relative abundance prior to administration. In some aspects, the methods comprise administering to the subject a composition comprising Bacteroides uniformis and / or Blautia sp., wherein the relative abundance of Bacteroides uniformis and / or Blautia sp. is increased in the subject compared to the relative abundance prior to administration. In some aspects, the methods comprise administering to the subject a composition comprising Bacteroides uniformis and / or Blautia sp., wherein Blautia sp. has a 16S rDNA sequence comprising SEQ ID NO: 1 or SEQ ID NO: 2, and wherein the relative abundance of Bacteroides uniformis and / or Blautia sp. is increased in the subject compared to the relative abundance prior to administration. In some aspects, the subject has autism spectrum disorder. In some aspects, the subject has autism spectrum disorder and an gastrointestinal distress. In some aspects, the composition increases the colon length in the subject. Disclosed herein are methods of treating a subject with inflammatory bowel disease. In some aspects, the methods can comprise administering to the subject any of the compositions disclosed herein, wherein the relative abundance of Bacteroides uniformis and / or Blautia sp is increased in the subject compared to the relative abundance prior to administration. In some aspects, the methods comprise administering to the subject a composition comprising Bacteroides uniformis and / or Blautia sp., wherein the relative Attorney’s Docket No.: 21101.0478P1 abundance of Bacteroides uniformis and / or Blautia sp. is increased in the subject compared to the relative abundance prior to administration. In some aspects, the methods comprise administering to the subject a composition comprising Bacteroides uniformis and / or Blautia sp., wherein Blautia sp. has a 16S rDNA sequence comprising SEQ ID NO: 1 or SEQ ID NO: 2, and wherein the relative abundance of Bacteroides uniformis and / or Blautia sp. is increased in the subject compared to the relative abundance prior to administration. In some aspects, the subject has autism spectrum disorder. In some aspects, the inflammatory bowel disease can be Crohn’s disease or ulcerative colitis. In some aspects, the subject has autism spectrum disorder and an inflammatory bowel disease. In some aspects, the composition increases the colon length in the subject. Disclosed herein are methods of preventing weight loss or maintain weight in a subject. In some aspects, the methods can comprise administering to the subject any of the compositions disclosed herein, wherein the relative abundance of Bacteroides uniformis and / or Blautia sp is increased in the subject compared to the relative abundance prior to administration. In some aspects, the methods comprise administering to the subject a composition comprising Bacteroides uniformis and / or Blautia sp., wherein the relative abundance of Bacteroides uniformis and / or Blautia sp. is increased in the subject compared to the relative abundance prior to administration. In some aspects, the methods comprise administering to the subject a composition comprising Bacteroides uniformis and / or Blautia sp., wherein Blautia sp. has a 16S rDNA sequence comprising SEQ ID NO: 1 or SEQ ID NO: 2, and wherein the relative abundance of Bacteroides uniformis and / or Blautia sp. is increased in the subject compared to the relative abundance prior to administration. In some aspects, the subject has autism spectrum disorder. In some aspects, the inflammatory bowel disease can be Crohn’s disease or ulcerative colitis. In some aspects, the subject has autism spectrum disorder and an inflammatory bowel disease. In some aspects, the composition increases the colon length in the subject. KITSIn some aspects, a kit is disclosed comprising Bacteroides uniformis and / or Blautia sp. treating a subject with gastrointestinal distress, treating a subject with inflammatory bowel disease, or preventing weight loss or maintain weight in a subject. In some aspects, the kits can also comprise a carrier. Attorney’s Docket No.: 21101.0478P1 EXAMPLES Example 1. Colitis reduces active social engagement in mice and is amelioratedby supplementation with human microbiota members Multiple neurological disorders are associated with gastrointestinal (GI) symptoms, including autism spectrum disorder (ASD), multiple sclerosis (MS) and Parkinson’s disease (PD). ASD, MS, and PD are However, it remains unclear whether GI distress itself can modify aspects of behavior. The results described herein show that mice that had experienced repeated colitis had reduced active social engagement, in the form of interacting with a novel mouse, even though signs of colitis were no longer present. Next, it was tested whether individuals with ASD harbor a microbiota that might differentially influence GI health. To this end, the microbiota from individuals with ASD and familial neurotypical (NT) controls were transplanted into mice followed by induction of colitis. Animals that harbored a microbiota from ASD individuals had worsened gut phenotypes. The enrichment of Blautia species in the familial NT controls was identified and an association between abundance of Bacteroides uniformis and reduced intestinal injury was observed. Oral treatment with either of these microbes reduced colon injury in mice. Finally, provision of a Blautia isolate from a NT control could ameliorate gut injury- associated active social engagement in mice. Collectively, the data demonstrate that past intestinal distress is associated with changes in active social behavior in mice that can be ameliorated by supplementation of specific members of the human microbiota. Multiple neurological disorders including ASD, MS and PD are known to be influenced by a combination of genetic, neurobiological, immunological and environmental factors. More recently, one of the environmental factors found to be involved in these diseases is the microbiota (Hsiao, E.Y. et al. Cell 155, 1451-1463 (2013); Sampson, T.R. et al. Cell 167, 1469-1480 e1412 (2016); Sharon, G. et al. Cell 177, 1600-1618 e1617 (2019); Cekanaviciute, E. et al. Proc Natl Acad Sci U S A 114, 10713- 10718 (2017); and Lee, Y.K., et al. Proc Natl Acad Sci U S A 108 Suppl 1, 4615-4622 (2011)). Many individuals that have these diseases are co-morbid for GI symptoms such as diarrhea, constipation, abdominal pain, reflux, and bloating which often correlates with the severity of neurological deficits (Martinez-Gonzalez, A.E. & Andreo-Martinez, P. Medicina (Kaunas) 55 (2019); Ullah, H. et al. Front Neurosci 17, 1225875 (2023); and McElhanon, B.O., et al. Pediatrics 133, 872-883 (2014)). Other GI dysfunctions, including reduced GI motility and increased gut permeability, have also been reported (Boukthir, S. et al. [Abnormalintestinal permeability in children with autism]. Tunis Med 88, 685-686 (2010); and de Attorney’s Docket No.: 21101.0478P1 Magistris, L. et al. J Pediatr Gastroenterol Nutr 51, 418-424 (2010)). Additionally, a large multicenter trial of over 14,000 individuals reported a higher incidence of inflammatory bowel disease (IBD) in individuals with ASD (Kohane, I.S. et al. PLoS One 7, e33224 (2012)). These data underscore the notion that intestinal factors, including the gut microbiota, might modify the presentation of neurological disease manifestations such as behavior. Several studies have identified differences in the microbiota between ASD-affected individuals and neurotypical (NT) controls (individuals without neurological, or psychiatric diagnoses), prompting further investigations into the modulatory effects of gut bacteria on behavior (Finegold, S.M. et al. Anaerobe 16, 444-453 (2010); Finegold, S.M. et al. Clin Infect Dis 35, S6-S16 (2002); Williams, B.L., et al. mBio 3 (2012); Gondalia, S.V. et al. Autism Res 5, 419-427 (2012); Kang, D.W. et al. PLoS One 8, e68322 (2013); and Kang, D.W. et al. Anaerobe 49, 121-131 (2018)). Indeed, commensal bacteria have been shown to affect a number of complex behaviors in several animal models (Sen, P. et al. Brain Behav Immun 106, 115-126 (2022); and Cryan, J.F. et al. Physiol Rev 99, 1877-2013 (2019)). In an open-label study, individuals with ASD that received a fecal microbiota transplant (FMT) from a NT donor had significant improvements in behavior and GI symptoms (Kang, D.W. et al. Microbiome 5, 10 (2017)). Moreover, transplantation of the microbiota from individuals with ASD, MS or PD into mice led to modifications of the respective disease (Sampson, T.R. et al. Cell 167, 1469-1480 e1412 (2016); and Cell 177, 1600-1618 e1617 (2019); and Cekanaviciute, E. et al. Proc Natl Acad Sci U S A 114, 10713- 10718 (2017)). Thus, there is evidence in animal models and human trials that the gut microbiota can modulate behavioral outcomes in a variety of neurological diseases. However, since many of these studies utilize genetic modifications associated with that particular disease, it is difficult to disentangle the effects of the gene, microbiota and / or intestinal inflammation on the behavioral outcome. As described herein, a model of repeated intestinal injury and microbiota transplantation was employed to test whether the microbiota harbored by individuals with a neuro-developmental disorder might directly influence GI distress, which could modify subsequent behavioral outcomes. FMT is currently being trialed as a therapy in several diseases; however, the complexity of the community of an FMT makes it difficult to obtain reproducible donor micobiotas, and there is the possibility of transferring pathobionts into the recipient. Thus, identification of specific microbiota members that can ameliorate GI symptoms and modify neurological manifestations will be important for future management of these disorders (Wekerle, H. Attorney’s Docket No.: 21101.0478P1 Acta Neurol Scand 136 Suppl 201, 22-25 (2017); Zhang, Y. et al. J Neuroimmunol 301, 83-87 (2016); and Kakoty, V. et al. Neurosci Lett 753, 135865 (2021). As described herein, a model of repeated intestinal injury and microbiota transplantation was used to test whether the microbiota harbored by individuals with a neuro-developmental disorder might directly influence GI distress, which could modify subsequent behavioral outcomes. The results show that past intestinal distress is associated with changes in active social behavior in male mice, as they spend less time interacting with an unfamiliar mouse than mice naïve to intestinal insult. The results also demonstrate that transplantation of the microbiota from individuals with ASD into mice is sufficient to induce worsened gut phenotypes upon colitis induction compared to mice colonized with microbiotas from familial NT controls. To determine the specific microbiota members that contribute to these phenotypes, the microbiota compositions were analyzed. The results show that there is an enrichment of Blautia species in the familial NT controls and association between Bacteroides uniformis abundance and reduced intestinal injury in mice. The results also show that oral treatment with B. uniformis or a NT control Blautia isolate reduces colitis severity and that provision of the Blautia isolate ameliorates colitis- associated active sociability reductions in mice. Animals that experience repeated colitis have decreased active social interactions. While there appears to be a clear connection between gut dysfunction and diseases of the CNS, it is unclear to what degree the intestinal ailments themselves contribute to behavioral abnormalities. A few studies have begun to test this in acute models of dextran sulfate sodium (DSS)-induced colitis. In these studies, animals exhibited increased anxiety- like behaviors and memory loss during the active phase of disease. These behavioral deficits were often reversed when the damaging agent was discontinued and the disease resolved (Nyuyki, K.D., et al. Front Behav Neurosci 12, 58 (2018); Reichmann, F. et al. Sci Rep 5, 9970 (2015); Dempsey, E., et al. Brain Behav Immun 80, 616-632 (2019); and Vecchiarelli, H.A. et al. Neuropsychopharmacology 46, 992-1003 (2021)). As animals actively experiencing intestinal injury develop diarrhea, stop grooming, become hunched, and lose significant amounts of weight, it is perhaps not surprising that they also have behavioral differences. However, most individuals with comorbid GI disease and behavioral deficits experience frequent bouts of intestinal dysfunction whereby symptoms can relapse and remit. One study did compare an acute and repeated model of DSS treatment and observed fewer behavioral abnormalities in animals having repeated disease (Matisz, C.E., et al. Physiol Behav 216, 112802 (2020)). However, behavioral responses Attorney’s Docket No.: 21101.0478P1 were still analyzed just one day after the last DSS treatment, when animals were still actively experiencing disease. To understand the link between repeated intestinal complications and behavioral outcomes, mice were treated with a 30-day time-course of repeated DSS, consisting of five days of 2.5-3.0% DSS treatment, ten days of regular water, followed by another 5 days of DSS and ten days of water. This model allows for control of the timing of intestinal damage, which is followed by periods when the intestines repair and animals regain the weight lost during the DSS treatment (Chassaing, B., et al. Curr Protoc Immunol 104, 15 2511-152514 (2014)). This model is also well known to increase gut barrier permeability, a feature associated with several neurological disorders, including ASD. At the end of the 30 days, a battery of behavioral tests were performed to measure anxiety- and depression- related responses, as well as compulsivity and sociability. Consistent with appropriate induction of disease, DSS-treated mice weighed significantly less over the entire course of observation (FIG.1A, 1B and FIGS. 7A, 7B), displayed reduced colon length (FIG.1C), and had elevated fecal lipocalin-2 levels (FIG.7C). Importantly, however, at this time, animals that experienced repeated GI injury did not exhibit significant differences in locomotor activity (FIG. 1D) or apparent signs of sickness, as they were appropriately groomed, had no diarrhea, and did not display a hunched posture or other general signs of disease such as inflammation of the eyes and swelling of the face as would be seen in the acute DSS injury model. In contrast to published findings during acute GI insult, no differences were observed in anxiety-like behavior as measured by the elevated plus maze and open-field tests (FIGS.7D to 7F). Moreover, no differences in compulsive or depressive-like responses were observed as measured by the marble-burying and the tail suspension tests, respectively (FIGS.7G-J). These results demonstrate that repeated GI disease does not globally impact behavior and that anxiety-like behavior might be associated with acute inflammation. To assess alterations in sociability, the three-chamber test was conducted. Both groups of mice entered the social chamber with the novel mouse more often than the control chamber (FIG.7K). However, animals that had experienced repeated GI insult spent less time actively sniffing and interacting with the novel caged mouse (FIG.1E), demonstrating that animals with intestinal injury display deficits in their propensity to engage in social interactions with unfamiliar mice. Overall, these data show that repeated GI insult is associated with abnormal social interactions in mice. Attorney’s Docket No.: 21101.0478P1 Microbiota transplantation from individuals with ASD alters intestinal phenotypes in mice. ASD is one of multiple neurological disorders with observed gastrointestinal comorbidities, and depending on the study, up to 85% of individuals with ASD also have GI complaints (Martinez-Gonzalez, A.E. & Andreo-Martinez, P. Medicina (Kaunas) 55 (2019)). While one group has demonstrated that transplantation of the microbiota from individuals with ASD can alter behavior in mice, the impact of the microbiota from individuals with ASD on intestinal health was not tested (Sharon, G. et al. Cell 177, 1600- 1618 e1617 (2019)). The data show that repeated GI insult is associated with a decreased propensity to engage socially, a characteristic feature of ASD. Thus, some individuals with ASD might harbor a microbiota that reduces intestinal health and subsequently modifies behavioral phenotypes. Based on this, it was determined whether the microbiota from individuals with ASD could alter disease severity after an acute course of DSS treatment. This model was chosen to screen several microbiotas for alterations in disease severity because it is reproducible, quick, and provides clear outcomes that are easy to assess in a large number of animals (Chassaing, B., et al. Curr Protoc Immunol 104, 152511-1525 14 (2014)). Fecal samples were collected from households containing at least one member with ASD, and other household family members were used as neurotypical (NT) controls. Use of household, familial samples better controls for some environmental, genetic and dietary differences that may also drive alterations in the microbiota (Song, S.J. et al. Elife 2, e00458 (2013); and Hajjar, J. et al. Res Sq (2023)). Five donor families were identified through the Utah Population Database (Table 2). ASD donors consisted of 4 males and 1 female while household control donors consisted of 4 females and 4 males. The household controls were either unaffected sibling controls or parents of the individuals with ASD (FIG.2 and Table 2).

[0002] Attorney’s Docket No.: 21101.0478P1 Table 2: Donor Diagnosis and key. ID Birth Gender DiagnosisYear g g ggg g g ID Family Donor Donor (in Note Attorney’s Docket No.: 21101.0478P1 4018022 5 ASD c 4018024 5 Sibling b offspring of these “humanized” breeders (referred to as H-F1 offspring) were provided DSS for 7 days3(FIG.8A). In this model, weight loss and colon shortening are two commonly analyzed parameters used for gross examination of wasting and intestinal damage. When the H-F1 animals receiving NT microbiotas or microbiotas from individuals with ASD are grouped together, there are no significant differences in colon shortening; however, animals receiving the microbiota from ASD individuals lost more weight when compared to animals receiving a microbiota from a neurotypical donor (FIGS. 2A-C). Yet, when each microbiota is treated as a single sample for weight loss, the effect size of weight loss in mice given a microbiota from patients with ASD is reduced (p=0.0627) (FIG. 8B). Analysis of the data when grouped by family revealed that the microbiota from all but one individual with ASD consistently worsens either weight loss, colon shortening or both when compared to the respective familial controls (FIGS. 2D-W). Animals colonized with the ASD microbiota from families 2-5 lost significantly more weight and / or had significantly shorter colons when compared to at least one of their household NT controls (FIGS.2H-W). Family 2 has a household control that has been diagnosed with ulcerative colitis, and indeed, it appears this microbiota leads to similar weight loss as one of the individuals with ASD (FIGS. 2H-K). Within family 3, the microbiota from the individual with ASD led to significant weight loss and colon shortening compared to the neurotypical mother (FIGS.2L-O) In family 4, mice colonized with the microbiota of the ASD donor led to a significant decrease in colon length when compared to a same-sex NT sibling, but not the parent (FIGS.2P-S). Family 5 contains a sex-matched sibling control without ASD and transplantation of this microbiota does not lead to as much weight loss as animals receiving the microbiota from the individual with ASD (FIGS. 2T-W). Thus, in most cases, microbiotas from individuals with ASD worsen GI symptoms. Collectively, these data demonstrate that the microbiota possessed by some individuals with ASD can exacerbate GI insult. Identification of human GI bacteria that reduce DSS injury. Donor input samples and large intestinal contents from 6-8-week-old offspring were subjected to 16S sequencing to interrogate their microbiotas. In this case, the source of the sample Attorney’s Docket No.: 21101.0478P1 (sequenced inputs of human feces or output from F1 progeny of colonized mice) strongly dictated community similarity and clustered together (FIGS. 3A, 3B). To characterize the microbiota structure in colonized mice, the human input samples were excluded and unweighted UniFrac distances were measured between mice colonized with the same microbiota compared to mice colonized with different microbiotas. UniFrac distances are smaller within microbiotas than between microbiotas (FIG.9A). When analyzing microbiotas from an individual family and including human donors, PCoA plots show distinct clustering by source and microbiota (FIG.3B). The plot’s vertical axis (PCoA axis 2; explaining 19.20% of variation) separates samples by microbiota and not by source. Taken together, the microbiotas of the recipient animals cluster together and more closely resemble the community of the donor sample than that of other animals transplanted with samples from different donors. When analyzing colonized mice via unweighted UniFrac, PCoA plots showed that microbiota composition seemed to cluster by donor family (FIG. 3C). By comparing UniFrac values within and between each family, it was found that the mean distance within each family is significantly less than between each other family (FIGS.9B-F). These data demonstrate that donor family strongly dictates community structure. These data support that transplantation of human microbiotas to animals maintains features of the human donor. Several reports have identified distinctions between microbiotas from ASD and NT individuals (Sharon, G. et al. Cell 177, 1600-1618 e1617 (2019); Kang, D.W. et al. PLoS One 8, e68322 (2013); and Kang, D.W. et al. Anaerobe 49, 121-131 (2018)). Transplantation of the microbiota from an individual with ASD into mice can worsen some behavioral outcomes demonstrating that the microbiota from an individual with ASD influences behavior abnormalities (Sharon, G. et al. Cell 177, 1600-1618 e1617 (2019)). Moreover, fecal microbiota transplantation (FMT) from NT into ASD patients is associated with a reduction in severity of behavioral abnormalities (Kang, D.W. et al. Microbiome 5, 10 (2017)). As microbes can influence GI function and GI function can influence CNS function, specific members of the microbiota were identified that correlated with intestinal phenotypes. Initially, animals were analyzed to determine if neurotype influenced community composition. By comparing unweighted UniFrac distances, it was found that donor neurotype also predicts microbiota structure; within-neurotype distance is smaller than between-neurotype distance (FIG.3D). There was also more distance within the NT- colonized mice than the ASD-colonized mice. Like previous reports from humans with ASD, it was found that mice colonized with ASD microbiotas had less Actinobacteria and Attorney’s Docket No.: 21101.0478P1 Firmicutes and more Proteobacteria (FIG.9G). Interestingly, when comparing individual taxa that were differentially abundant between neurotypes, one was significantly different. This ASV was a Eubacterium sp. that was detected in animals colonized from ASD donors (FIG.9H). While this microbe was found in four of the seven cohorts of mice colonized with the ASD microbiotas, it was not detected in any NT-colonized mice. This finding is similar to a recent report that individuals with ASD had high Eubacterium prior to receiving an FMT (Li, N. et al. Front Cell Infect Microbiol 11, 759435 (2021)). Linear regression was performed between mean abundance of individual taxa and weight or colon length of the transplanted animals. From these regressions, multiple ASVs, including an Enterobacteriaceae, were identified that were negatively associated with final weight (FIG.9I) and thus were increased in abundance in animals that lost the most weight during DSS treatment. When looking at ASD- colonized mice, the organism that was identified to be positively associated with final weight and a trending relationship with colon length was Bacteroides uniformis (FIGS. 3E and 3F). This data showed that B. uniformis is associated with protection from intestinal injury in ASD-colonized mice. In humans, the presence of B. uniformis in healthy volunteers distinguishes them from individuals with irritable bowel syndrome and ulcerative colitis, and individuals with Crohn’s disease have a lower abundance of B. uniformis, further demonstrating the association of B. uniformis with less intestinal disease (Noor, S.O. et al. BMC Gastroenterol 10, 134 (2010); and Dicksved, J. et al. ISME J 2, 716-727 (2008)). The microbiota in humans is known to have high interpersonal variability and it is likely that many microbiota-influenced diseases are not a result of a gain or loss of a single universal organism. Based on this, a more personalized analysis of the microbiota from a single family was carried out to identify organisms of interest. Initially, the focus was on the microbial differences in family 3 as the intestinal disease severity was most distinct between the NT control and ASD colonized mice (FIGS. 2L-2O). Sequencing of the two microbiotas from this family showed that distinct members of the genus Blautia were differentially abundant between the NT control and ASD colonized animals (FIG.3G). Interestingly, Blautia species have been reported to be significantly reduced in individuals with ASD that are also comorbid for GI disease (Luna, R.A. et al. Cell Mol Gastroenterol Hepatol 3, 218-230 (2017)). Other families were analyzed to determine whether there are differences in Blautia. When regressing Blautia sp. frequency against weight loss, a significant relationship was not observed (FIG. 9J). However, when analyzing the microbiotas from families individually, there is a significant difference in Blautia species Attorney’s Docket No.: 21101.0478P1 across multiple families. Indeed, in the families, ASD colonized mice have less Blautia sp. than either a sibling (families 2 and 3) or parental (families 1, 4 and 5) control (FIG.9K). Thus, personalized analysis in animals transplanted with human microbiota can reveal organisms of interest. The transplantation studies have highlighted two candidate bacterial organisms that are significantly correlated with worsened intestinal outcomes in mice and appear to be reduced in individuals with ASD and GI problems, demonstrating that these organisms can reduce intestinal injury or disease. Oral treatment with B. uniformis reduces intestinal disease in mice. To determine how B. uniformis modifies intestinal injury, animals were orally gavaged with 107CFU / day of B. uniformis two weeks prior to initiation of acute DSS injury. B. uniformis had little effect on animals in the absence of DSS treatment, providing evidence that oral gavage of this bacteria is well tolerated. However, during DSS injury while B. uniformis treated animals lost a similar amount of weight compared to mock-treated animals, B. uniformis treated animals had significantly longer colons and less fecal lipocalin-2 (FIGS. 4A-C). Blinded histological analysis also showed that B. uniformis treated mice had similar immune cell infiltrate into the tissue yet had significantly decreased crypt loss (FIGS.4D, 4E and FIG.10). Based on this data, increased abundance of B. uniformis identified in NT individuals is predicted to protect from intestinal injury and inflammation. Blautia sp. from a NT individual reduces intestinal injury in humanized mice. The analysis of family 3 revealed distinct differences in Blautia species between the NT and the ASD individuals. Therefore, a culture collection of microbes from NT-colonized mice was assembled to isolate Blautia species that were associated with reduced intestinal disease. Multiple isolates of Blautia were cultured and one with 99% 16S rDNA similarity to the Blautia overrepresented in the maternal sample (now referred to as Blautia-NT) was identified. To test Blautia-NT’s influence on disease severity, germfree mice were colonized with the original family 3 ASD and NT microbiotas. Two weeks before DSS, a subset of these animals were gavaged with 107CFU / day of Blautia-NT. Mice colonized with the ASD microbiota again lost significantly more weight and had shorter colons than the NT-colonized mice (FIGS.5A-C). Additionally, histological analysis was performed on these animals and identified that animals colonized with the ASD microbiota had significantly higher disease scores that indicated greater intestinal injury (FIGS.5D, 5E and FIG.11). However, oral treatment of ASD colonized animals with Blautia-NT, significantly protected animals from weight loss, colon shortening and crypt loss (FIGS. 5A to 5E). The Blautia-NT treatment did not affect disease in mice colonized with the NT Attorney’s Docket No.: 21101.0478P1 microbiota. The lack of effect might be due to either the already high levels of Blautia in the colonized mice or the already-limited disease conferred from this microbiota. To test this, Blautia-NT was orally gavaged into wild-type SPF mice prior to induction of DSS colitis. The SPF mouse colony lacks this Blautia strain and possesses a microbiota that leads to moderate colitis (FIG. 4). Oral treatment with Blautia-NT into SPF mice also potently protected from colitis severity. Indeed, animals treated with Blautia-NT had longer colons, reduced lipocalin-2 levels and reduced intestinal damage (FIGS.5E-H). These demonstrate that Blautia-NT can reduce intestinal disease in multiple microbiota backgrounds that are conducive to moderate colitis and lack Blautia sp. Blautia-NT ameliorates intestinal injury-associated asocial behavior. The data demonstrate that repeated intestinal injury is associated with reduced social interactions in mice. Two organisms from the human microbiota were identified that reduce DSS-induced intestinal injury, so it was tested whether these organisms can be used to ameliorate intestinal injury-induced reductions in social behavior. To test this, the three-chamber test was performed after treating animals orally with either Blautia- NT or B. uniformis during repeated, intermittent DSS insult. Again, animals that had experienced repeated intestinal damage had no differences in locomotion but were significantly less interactive with the novel mouse when compared to age and sex-matched treatment naïve mice (FIGS. 6A, 6B). However, while mice orally gavaged with B. uniformis had no significant changes (p=0.181) in sociability, animals treated with Blautia-NT displayed significantly increased social engagement with novel animals compared to animals that had experienced intestinal insult (FIG.6B). Collectively, the data demonstrate that intestinal injury alone can influence certain aspects of behavior and that some individuals with ASD might lack members of the microbiota that can protect or improve intestinal complications and worsen behavioral outcomes. A recent literature review analyzed the data from human studies involving GI symptoms in ASD and identified that over 70% of these studies reported statistically significant differences in the occurrence of GI complications in individuals with ASD, supporting the high prevalence of intestinal abnormalities in this behavioral disorder35. Similar observations have been made for other neurological diseases, including Parkinson’s disease and multiple sclerosis (Wekerle, H. Acta Neurol Scand 136 Suppl 201, 22-25 (2017); and Zhang, Y. et al. J Neuroimmunol 301, 83-87 (2016)). These ailments involve complex interactions between genetics, environment, diet, and the immune and nervous systems; thus, understanding what components of these diseases influence behavioral Attorney’s Docket No.: 21101.0478P1 symptoms becomes difficult. The use of mouse models can help to tease apart these differences, and several investigations have used genetic models, whereby animals possess polymorphisms or deletions in genes known to be associated with the disease (Sampson, T.R. et al. Cell 167, 1469-1480 e1412 (2016); Cekanaviciute, E. et al. Proc Natl Acad Sci U S A 114, 10713- 10718 (2017); Hsiao, E.Y. et al. Cell 155, 1451-1463 (2013); and Golubeva, A.V. et al. EBioMedicine 24, 166-178 (2017)). However, in these models, the genetic deletions are often not specific to the brain and could also influence the developing gut and microbiota. Thus, a major question left unanswered is whether microbiota-driven GI complications alone can influence behavioral abnormalities. On this basis, a model of repeated gut injury would allow to definitively test this. The use of the DSS model is a sufficient model for this purpose because it allowed specific timing of the gut injury and a period of recovery prior to behavioral testing. This is an important distinction from the few studies that have looked at behavior in the acute DSS model where animals are actively losing weight, have stark diarrhea, and often appear moribund, which would be expected to manifest in behavioral differences due to extreme sickness (Talley, S. et al. J Neuroinflammation 18, 263 (2021)). Additionally, this model can be performed in wild-type animals and therefore does not have the complication that a specific genetic deficiency or early life perturbation may also indirectly influence gut or brain activity. Using this model, it was observed that while animals that experienced repeated gut injury entered the social chamber as often as non-DSS mice, they displayed decreased active social engagement, in the form of sniffing and interacting, with an unfamiliar mouse. This demonstrates that intestinal distress might modify the way an individual engages socially with others. The reason why intestinal distress modifies social engagement is unclear. It is possible that despite having the appearance of health, the animals might still be experiencing visceral pain and this could modify their behavior. These results show that GI distress in individuals with neurological diseases, such as ASD, might modify their behavioral symptoms and that treating gut complications could ameliorate some behavioral abnormalities seen in neurological diseases. Given the wealth of literature demonstrating the direct effects of the gut microbiota on intestinal wound repair, inflammation, and severity of disease, such as in IBD, it was tested whether the microbiota harbored by individuals with ASD can influence severity of GI insult (Ost, K.S. & Round, J.L. Annu Rev Microbiol 72, 399-422 (2018)). One study that transplanted ASD microbiota into naïve germ-free animals observed no differences in one parameter of GI health, intestinal permeability, based on the microbiota composition Attorney’s Docket No.: 21101.0478P1 alone3. However, modeling intestinal manifestations in mice requires a variety of factors. Indeed, in studies testing the role of the microbiota in induction of IBD, transplantation of the microbiota from IBD patients alone is not sufficient to elicit disease in mice and requires a genetic or chemical induction factor (Britton, G.J. et al. Immunity 50, 212-224 e214 (2019)). Thus, the DSS was used to test the ability of the microbiota harbored by individuals with ASD to influence symptoms associated with intestinal distress. Of note, the individuals from this study were also surveyed for GI complaints. Consistent with the literature, most individuals with ASD self-reported some sort of GI complaint with the most common being reflux and a few reported abdominal pain and / or constipation (Table 2 and Table 3). One individual in this study had a clinical diagnosis of inflammatory bowel disease (IBD), ulcerative colitis, and this was one of the NT controls, whose microbiota showed exacerbated inflammation when transplanted into mice. The data showed that, in general, the microbiota harbored by NT individuals did not exacerbate intestinal outcomes to the same degree as the microbiota from ASD individuals, demonstrating that some individuals with ASD harbor a microbiota that potentiates GI distress. More recent work in the microbiota field now supports that many gut diseases, such as IBD and obesity, can result from the loss of beneficial organisms as opposed to the acquisition of pathogenic ones (Petersen, C. et al. Science 365 (2019). Based on this, organisms were identified that were reduced in animals that experienced worsened disease. This analysis was performed in two ways: the first, by combining the microbiotas together and stratifying based on the severity of disease; and the second, via a more personalized analysis of a single household. These two methods identified that the two organisms, B. uniformis and Blautia sp., were positively correlated with less weight loss and / or colon length. These two organisms have not been mechanistically studied in the context of ASD; however, they have been noted in several observational studies of the microbiota in ASD. In mouse models of ASD, Blautia species are reduced in animals genetically predisposed to ASD18. In humans with ASD, Blautia species are continually demonstrated to be depleted in ASD microbiotas and enriched in NT individuals and Blautia species specifically were found to be depleted in individuals with both ASD and GI complaints35. B. uniformis, however, has been shown to be enriched in both NT and ASD individuals depending on the study and thus is not clearly connected with ASD. However, in an animal study, treatment with B. uniformis resolved the behavioral abnormalities observed in mice possessing haploinsufficiency of the chromodomain helicase DNA binding protein (CHD8), one of the top genes associated with ASD (Yu, Y. et al. Nat Commun 13, 1151 Attorney’s Docket No.: 21101.0478P1 (2022)). Even so, parameters of GI health were not measured in this study; thus, it is unclear whether B. uniformis modified local intestinal manifestations. The data demonstrate that both Blautia-NT and B. uniformis can ameliorate pathology and weight loss associated with gut injury induced by DSS. Interestingly, the worsened colitis severity associated with colonization of animals with the microbiota from one ASD individual could be resolved by oral gavage with a Blautia isolated from the NT mother, highlighting that individuals with neuro- developmental disorders might lack specific organisms that promote GI health. Moreover, in the study described herein, Blautia-NT significantly improved the deficit in active social engagement associated with induction of GI insult. B. uniformis also somewhat improved GI insult-associated social behavior abnormalities. A previous study using the MIA model of ASD was able to ameliorate some of the behavioral abnormalities associated with this model using oral treatment of Bacteroides fragilis1. Prior to this study, B. fragilis had been shown to improve multiple models of intestinal colitis in mice and induce anti-inflammatory responses within the intestine (Round, J.L. & Mazmanian, S.K. Proc Natl Acad Sci U S A 107, 12204- 12209 (2010); Round, J.L. et al. Science 332, 974-977 (2011); and Mazmanian, S.K., Round, J.L. & Kasper, D.L. Nature 453, 620-625 (2008)). Thus, collectively these studies highlight that provision of specific members of the microbiota that are lacking in individuals with neurobehavioral problems might improve their GI health and also improve certain aspects of their behavior. This could extend to a variety of diseases whereby GI complications are implicated. Indeed, individuals with IBD have been reported to have increased anxiety, depression, and asocial behavior. Future studies will be aimed at identifying the mechanism by which Blautia-NT is able to ameliorate gut injury- associated behavioral abnormalities. Collectively, these studies demonstrate that individuals with neuro-developmental diseases can harbor a microbiota that promotes intestinal inflammation that could exacerbate specific aspects of their behavioral outcomes. FMT is being explored as a therapy for many of these diseases; however, the complexity of the community within an FMT makes it difficult to ensure reproducible transplants over time and has the possibility of transplanting unknown pathobionts to the recipient. Thus, identification of specific organisms that can ameliorate GI distress would be useful in this regard. Two such microbes, Blautia-NT and B. uniformis, were identified herein that ameliorate GI distress in mice. Thus, the use of these bacteria can be used in targeted microbiota replacement therapy. Attorney’s Docket No.: 21101.0478P1 Table 3: Donor Diagnosis and Medical History. ID Medical Medications1281021 Seasonal Allergies; None1281011Ibu rofen; Multi-Vit; As irin;fy;r; ; Attorney’s Docket No.: 21101.0478P1 nissen fundopliation at Materials and Methods. Mice.3-to-4-week-old male C57BL / 6 mice were purchased from Jackson Labs and housed / tested in one of 3 mouse facilities at the University of Utah. The animals were housed in a climate-controlled facility with 12- hour light / dark cycles, with ad libitum access to standard mouse chow and water. Germfree C57BL / 6 mice were maintained in gnotobiotic isolators in the germfree mouse facility. Animals were housed in a climate-controlled facility with 12-hour light / dark cycles, a temperature of 22°C and 22-30% relative humidity. Mice had ad libitum access to standard mouse chow (Teklad Rodent Diet 2920X, inotiv) and water. Mice were housed in cages with 2-5 mice, and cages were changedevery 2 weeks. Germfree C57BL / 6J mice were maintained in gnotobiotic isolators or Tecniplast cages in the germfree mouse facility under similar conditions, with autoclaved standard mouse chow. DSS induced intestinal injury model.2.5%–3.0% DSS (36,000-50,000 MW, Fisher Scientific), depending on mouse facility, was diluted in water and given to mice as the sole source of drinking water to induce intestinal distress. For repeated injury DSS water was administered for five days, then mice were given ten days of regular water, then five days of DSS, and finally ten more days of regular water. Mice were then analyzed at this time point (Day 30) or used for behavioral testing. For acute DSS schedule, mice were given 2.5% DSS in their drinking water for 6 to 7 days and assayed daily for change in weight. Histological Analysis. Whole colons were isolated and fixed in formaldehyde followed by 70% ethanol. Paraffin embedded sections were cut longitudinally at 5 µm and stained with hematoxylin and eosin. The entire length of the colon from just under the cecum Attorney’s Docket No.: 21101.0478P1 to the rectum was analyzed and percent of crypt loss and percent of colon affected by inflammation was also taken into consideration. Therefore, each animal received a score for crypt loss and immune cell aggregation as well as the percent of the colon affected. For crypt loss severity a score of 0-3 was given (0=no crypt loss; 1=mild crypt loss, most crypts still visible with a few areas effected; 2=medium severity, greater crypt loss, fewer crypts visible in large areas; 3=very large areas of total crypt loss, places where crypts are completely gone). For immune cell aggregation: each was given from 0-3 that takes into account the levels of immune cells that are present within the lamina propria (0=no evidence of inflammatory infiltrate; 1=very low level of cells infiltrating into the tissue; 2= clear infiltrating lymphocytes into epithelial tissue; 3= large boluses of inflammatory infiltrates that correspond with areas a crypt loss). The percentage scoring was as follows: 0=no area affected; 0.5=1-5%; 1=5-20%; 1.5=20-30%; 2=30-45%; 2.5=45-60%; 3:=60-70%; 3.5=70- 80%; 4=>80%. This was the same scoring system used for crypt loss and inflammation. Behavioral Assays. Mice given repeated DSS treatment, or control mice were allowed two hours to acclimatize to the behavioral assay laboratory each of the two days prior to the beginning of testing. Mice were subjected to a battery of behavioral tests, including: three- chamber, open field, novel object recognition, elevated plus- maze, tail suspension, pre-pulse inhibition and marble burying tests. In each test, isopropyl alcohol was used to thoroughly clean the in-use apparatus between trials. This was done to remove the any remaining odors; any confounding effects. Three-Chamber Test. This test was performed on a three-chamber opaque acrylic box. An empty central compartment connects with two lateral compartments (20 x 20 cm). Two cylindrical wire cup enclosures (10x6 cm in diameter) were placed in the center of the lateral compartments respectively containing an age- and weight-matched male foreign conspecific (acclimated extensively to the enclosures before testing) or an inanimate object of equal size. The test mouse was acclimated to the empty apparatus and allowed to freely explore for 10 min, 24 h prior to testing. The day after, the mouse was placed in the central compartment and allowed to explore the social and non-social compartments for 10 min. Placement of the wire cup enclosures was counterbalanced across treatments. Behavioral measures include the number of social approaches and the duration of social investigation / interaction. Transitions between compartments and active sniffing behavior directed toward counterpart / object were hand-scored offline. Social / object contacts were defined as active sniffing, pawing, and touching of the experimental subject in proximity (<1 cm) to the circular edge of the enclosure. Attorney’s Docket No.: 21101.0478P1 Open Field Test. Animals were placed in the center of a black Plexiglass open field area (40 x 40 x 40 cm) and allowed to explore freely for 5 minutes. Horizontal locomotor activity and spontaneous behaviors were scored and analyzed using behavioral tracking software (EthoVision XT). Novel Object Recognition Test. Mice were individually acclimatized to Makrolon cages for 15 min each. The day after, animals were exposed to two novel black plastic cylinders (8 cm tall × 3.5 cm in diameter), affixed to the floor and symmetrically placed at 6 cm from the two nearest walls. Mice were placed in a corner, facing the center and at equal distance from the two objects. Their start position was rotated and counterbalanced for each treatment throughout the test. Twenty-four h later, mice were placed in the same cage for long-term memory testing. One of the cylinders was replaced by a novel plastic rectangular block (6 cm tall × 3 × 3cm), which was placed in a counterbalanced fashion to avoid experimental bias. Behaviors for both sessions were videotaped for 15 min. Analysis included the number and total duration of exploratory approaches between novel and familiar objects. Exploration was defined as sniffing or touching either of the two objects with the snout; sitting on the object was not considered exploration. In the second exploration trial, an object exploration index was calculated as the ratio of the duration of the exploratory approaches targeting the novel objects over the time of exploration of both objects. Elevated Plus-Maze Test. A black Plexiglas apparatus with a light grey floor and featured two open arms (25 × 5 cm) and two closed arms (25 × 5 × 5 cm) that extended from a central platform (5 × 5 cm) at 60 cm from the ground. Mice were placed individually in the center square facing an open arm and allowed to explore the maze for 5 min. Behavioral analysis was performed by an observer unaware of condition, and included the following parameters: time spent in open and closed arms and in the central platform; number of open and closed arm entries; total entries; stretch-attend postures; head dips. An arm entry was counted when all four paws were inside the arm. Tail Suspension Test. The tail suspension test was performed as described elsewhere (Scott et al., 2008). Mice were individually suspended by the tail using medical tape affixed to a hook, at 30 cm from the floor. Environmental light was kept at 300 lux. Animals were videorecorder for 6 min, and the duration of immobility (s), the latency to immobility (s) and number of fecal boli were measured. Marble Burying Test. Mice were allowed to habituate to a sawdust filled cage for 10 minutes. At the end of this phase, the mouse was briefly removed and 24 glass marbles were placed on the surface of the cage at even distances. The animal was then reintroduced into the Attorney’s Docket No.: 21101.0478P1 cage and its behavior was monitored for the following 10 min. The number of digging bouts, the overall digging duration and the number of buried marbles were scored. A marble was considered buried if at least two- thirds of its surface area was covered in sawdust. Colonization with Human Microbiotas. Families were selected that contained at least one individual diagnosed with ASD and gastrointestinal complaint. Information regarding donor health, disease, and medication usage was collated (Tables 2, 3). Fecal samples were collected and dated by donors and stored in their freezers until pickup. After collection, bulk fecal samples were stored at -80°C until processing and colonization into mice. Colonization of mice was based off of protocol (Goodman, A.L. et al. Proc Natl Acad Sci U S A 108, 6252- 6257 (2011)). Fecal samples were allowed to thaw at room temperature and suspended in reduced PBS at 15 g / ml conical tubes. Samples were vortexed for 5 minutes and then given 5 minutes to allow solid particles to precipitate at the bottom of 15 ml conical tubes.200 mL aliquots of the suspended liquid fractions were then gavaged into germfree mice. Mice were removed from gnotobiotic isolators and immediately inoculated with human microbiotas, and then housed in secured Tecniplast Iso-cages with HEPA filters, segregated by microbiota sample. C57BL / 6 mice were utilized for their availability as GF mice, as well as their tractability for potential, future genetic manipulation. 16S rRNA Gene Sequencing. Fecal input samples and large intestinal luminal contents were collected for 16Ss sequencing of bacterial communities. DNA was isolated from contents using Zymo Quick-DNA Fecal / Soil Microbe 96 Magbead kit according to manufacturer’s instruction. Fluorometric measurement (Qubit) was then used to quantify and then normalize DNA concentrations used as templates in PCR. A single round of PCR was performed in triplicate using custom 16S targeting primers (below) on the 3’ end of long oligonucleotides including the 8nucleotide sample-specific barcode and Illumina adapter sequences (Kozich, J.J., et al. Appl Environ Microbiol 79, 5112-5120 (2013)). Both amplify V3 and V416S regions and used the same set of barcodes but employed different 16S rRNA gene targeting primer sequences. One run included fecal samples from colonized mice and all familial donors and utilized the 16S targeting sequences with 2 nucleotide pad (underlined) 5’-TGCCTACGGGNBGCASCAG-3’ (SEQ ID NO: 3) and 5’-GCGACTACNVGGGTATCTAATCC-3’ (SEQ ID NO: 4) (FIGS.3A-3F and FIG. 9A). The other run included family 3 donors and mice colonized with family 3 and utilized the 16S targeting sequences with 2 nucleotide pad (underlined) : 5’- TAGGGRGGCWGCAGTRRGG-3’ (SEQ ID NO: 5) and 5’- TTCTACHVGGGTATCTAATCCTGTT-3’ (SEQ ID NO: 6) (FIG.3G). Gel electrophoresis Attorney’s Docket No.: 21101.0478P1 was utilized to determine successfulness of PCRs, triplicates combined and PCR cleanup was performed using Axygen Magprep PCR cleanup kit according to manufacturer’s instructions. PCR products were then quantified using QuantIT picogreen (Invitrogen) and these final sequence libraries were evenly multiplexed. Samples were submitted to the Genomics Core at the University of Utah.5% PhiX spike was included and samples sequenced on Illumina Miseq with paired end 300 cycle sequencing. Analysis of 16s Data. Analysis of 16s data was performed with QIIME and QIIME2 utilizing the Center for High Performance Computing at the University of Utah. Cutdapt trim- pairs was used to remove primers from demultiplexed sequences. Vsearch join-pairs was used to join paired-end sequencing reads. Quality-filter q-score-joined was used to remove low quality reads (with a minimum PHRED score of 10). Deblur denoise-16s was used for quality control. Vsearch uchime-denovo was used to filter chimeras. Rooted Phylogenetic tree was assembled using phylogeny align-to-tree-mafft-fasttree pipeline. Samples were then rarefied to 10,000 reads by using feature-table rarify. To determine beta-diversity metrics between microbiota samples, the diversity core-metrics-phylogenetic pipeline was used. Unweighted UniFrac distances were used to compared beta-diversity between samples. To determine if individual taxa were differentially abundant between samples, we utilized the composition ancom (Analysis of Composition of Microbiota). Before ANCOM, taxa were collapsed and pseudocounts added to allow for analysis at different taxonomic levels. Culture Collection and Blautia Isolation. Feces collected from mice colonized with the microbiota 1306012 were collected and used to assemble a culture collection (Goodman, A.L. et al. Proc Natl Acad Sci U S A 108, 6252- 6257 (2011)). Feces were plated on GMM medium in an anaerobic chamber. Colonies were harvested from the plates and frozen for further use. Dilutions of frozen stocks were performed to determine the cell concentration. Using this calculation, cells were diluted into 96 well plates at the proper concentration to maximize the number of wells that contain 1 bacterial cell. These plates were allowed a week for growth to occur. Turbid wells were then subject to 16s sequencing and preserved in glycerol at -80°C. Treatment with Bacterial Supplements. Frozen stocks of either Blautia sp. or Bacteroides uniformis were thawed, spun down at 5,000g for 5 minutes and suspended in reduced PBS. Mice were then gavaged with 107CFU of bacteria beginning two weeks before DSS treatment, as well as during the DSS treatment time-course. For the acute DSS time- course, mice were gavaged daily the indicated bacterial stock, for the repeated time-course experiments, mice were gavaged every two to three days with bacteria. Attorney’s Docket No.: 21101.0478P1 Statistics and reproducibility. Mouse sample sizes were chosen based on either those utilized in similar studies and / or availability of mice. The latter is true for experiments that utilized age-matched offspring of breeder pairs colonized with human microbiotas. In these experiments, male offspring in each age-matched litter were utilized. Follow up behavioral study sample sizes were estimated using the calculated Eta square from the original set of results. Randomization was utilized throughout this work, specifically in selecting GF mice for colonization with human microbiotas, in selecting which mice were to receive which treatments in colitis experiments, and the order in which mice were behaviorally tested. Blinding was utilized in both scoring behavioral testing and histological sections. Due to the higher prevalence of ASD in male humans and better susceptibility to DSS than females, male mice were selected for analysis. No data were excluded from the analyses. Generally, experiments were repeated twice and were reproducible: colitis social deficits were observed multiple times, and rescue of disease with bacterial treatment was also replicated in multiple experiments. The Blautia sp. JLR.GB0024 genome assembly and raw reads have been deposited in the NCBI database under accession number PRJNA952791. The 16S rRNA gene sequence data and associated metadata is available under NCBI BioProject accession number PRJNA952791.

Claims

Attorney’s Docket No.: 21101.0478P1 CLAIMS WHAT IS CLAIMED IS:

1. A composition comprising Bacteroides uniformis or Blautia sp., and a carrier.

2. The composition of any of the preceding claims, wherein the composition comprisesat least 1x104cells of each bacterial strain.

3. The composition of any of the preceding claims, wherein a single dosage of thecomposition comprises between 1x104and 1x1010cells of each bacterial strain.

4. The composition of any of the preceding claims, wherein the composition is capableof preventing weight loss or maintaining weight in a subject.

5. The composition of any of the preceding claims, wherein the composition is capableof increasing colon length in a subject.

6. The composition of any of the preceding claims, further comprising apharmaceutically acceptable carrier.

7. The composition of any of the preceding claims, wherein the composition is frozen.

8. The composition of any of the preceding claims, wherein the composition is a solid.

9. The composition of any of the preceding claims, wherein the composition is a liquid.

10. The composition of claim 9, wherein the liquid is concentrated liquid.

11. The composition of claim 9, wherein the liquid is a dilute liquid.

12. The composition of preceding claims, wherein the composition is capable of replacingmicrobiota of a subject with a disease or disorder associated with an imbalanced microbiota.

13. The composition of claim 12, wherein the imbalanced microbiota is a decrease inBacteroides uniformis and / or a decrease of Blautia sp.

14. The composition of claim 12, wherein the disease or disorder is inflammatory boweldisease or gastrointestinal distress.Attorney’s Docket No.: 21101.0478P1 15. The composition of any of the preceding claims, wherein the composition isadministered in a form selected from the group consisting of powder, granules, a ready-to-use beverage, food bar, an extruded form, capsules, gel caps, and dispersible tablets.

16. A method of treating a subject with gastrointestinal distress, the method comprisingadministering to the subject the composition of any of claims 1-15.

17. A method of treating a subject with inflammatory bowel disease, the methodcomprising administering to the subject the composition of any of claims 1-15.

18. A method of preventing weight loss or maintain weight in a subject, the methodcomprising administering to the subject the composition of any of claims 1-15.

19. The method of any one of claims 16-18, wherein the subject has been identified asbeing in need of the treatment.

20. The method of any one of claims 16-19, wherein the subject has autism spectrumdisorder.

21. The method of claim 17, wherein the inflammatory bowel disease is Crohn’s diseaseor ulcerative colitis.

22. The method of any one of claims 16-21, wherein the step of administering thecomposition comprises delivering the composition to at least a stomach, a small intestine, or a large intestine of the subject.

23. The method of any one of claims 16-22, wherein the composition is administeredorally.

24. The method of one of claims 16-23, wherein the subject is a human.

25. The composition or method of any of the preceding claims, wherein the cells of thecomposition are active.

26. The method of any of preceding claims, wherein the composition is for replacingmicrobiota of a subject with a disease or disorder associated with an imbalanced microbiota.

27. A composition comprising a supernatant from Bacteroides uniformis or Blautia sp.Attorney’s Docket No.: 21101.0478P1 28. A composition comprising a Bacteroides uniformis or a Blautia sp.

29. The composition of any of the preceding claims, wherein Blautia sp. has the sequenceof SEQ ID NO: 1 or SEQ ID NO:

2.

30. A method of treating a subject with gastrointestinal distress, the method comprisingadministering to the subject the composition of any of claims 1-15, 25, 27, or 28, wherein the relative abundance of Bacteroides uniformis and / or Blautia sp. is increased in the subject compared to the relative abundance prior to administration.

31. A method of treating a subject with inflammatory bowel disease, the methodcomprising administering to the subject the composition of any of claims 1-15, 25, 27, or 28, wherein the relative abundance of Bacteroides uniformis and / or Blautia sp. is increased in the subject compared to the relative abundance prior to administration.

32. A method of treating preventing weight loss or maintain weight in a subject, themethod comprising administering to the subject the composition of any of claims 1-15, 25, 27, or 28, wherein the relative abundance of Bacteroides uniformis and / or Blautia sp. is increased in the subject compared to the relative abundance prior to administration.

33. The method of any one of claims 30-32, wherein the subject has been identified asbeing in need of the treatment.

34. The method of any one of claims 30-33, wherein the subject has autism spectrumdisorder.

35. The method of claim 31, wherein the inflammatory bowel disease is Crohn’s diseaseor ulcerative colitis.

36. The method of one of claims 30-35, wherein the step of administering thecomposition comprises delivering the composition to at least a stomach, a small intestine, or a large intestine of the subject.Attorney’s Docket No.: 21101.0478P1 37. The method of any one of claims 30-35, wherein the composition is administeredorally.

38. The method of any one of claims 30-37, wherein the relative abundance of at least oneof species of Bacteroides uniformis and / or Blautia sp. is increased by 5%.

39. The method of one of claims 30-38, wherein the subject is a human.

40. The composition or method of any of the preceding claims, wherein the cells of theconsortia are active.

41. The method of any one of claims 30-39, wherein the composition is for replacingmicrobiota of a subject with a disease or disorder associated with an imbalanced microbiota.