Ba strain and use thereof in inflammatory lesions of colon

Abstract

Bifidobacterium adolescentis strain ibiome027 and the use thereof in inflammatory lesions of the colon. The strain exhibits good effects in DSS-induced acute colitis and chronic colitis, TNBS-induced acute colitis, and TNF ΔARE mice, expands the clinical choices for the treatment of inflammatory lesions of the colon, and has broad prospects.

Description

A BA strain and its application in inflammatory lesions of the colon Technical Field

[0001] This invention relates to the field of biotechnology, specifically to a strain of Bifidobacterium adolescentis, ibiome027, and its application in inflammatory lesions of the colon. Background Technology

[0002] Inflammatory bowel diseases can be caused by organisms such as bacteria, fungi, viruses, parasites, and protozoa, as well as by allergic reactions and physical and chemical factors. Based on the etiology, they can be divided into specific colitis and nonspecific colitis. The former mainly refers to infectious colitis, ischemic colitis, pseudomembranous colitis, and radiation colitis, while the latter mainly refers to inflammatory bowel diseases, including ulcerative colitis and Crohn's disease. The clinical symptoms of colitis lack specificity and often manifest as diarrhea, abdominal pain, mucus and bloody stools, tenesmus, and are often accompanied by weight loss and fatigue. The condition is prone to recurrence, severely impacting the patient's quality of life.

[0003] Inflammatory bowel disease (IBD) is a chronic inflammatory bowel disease characterized by symptoms such as rectal bleeding, abdominal pain, diarrhea, or indigestion. Its pathogenesis is complex, involving genetic factors, mucosal barrier dysfunction, innate and adaptive immunity, and alterations in gut microbiota composition. In recent years, increasing research has demonstrated the important role of gut microbiota in the occurrence and development of IBD, showing therapeutic potential for IBD.

[0004] Bifidobacterium adolescentis is a Gram-positive, non-spore-forming bacillus widely distributed in the human gut and is one of the important microorganisms for maintaining gut health. It has various physiological functions, such as regulating the balance of gut microbiota, enhancing immunity, and inhibiting the growth of harmful bacteria. Furthermore, Bifidobacterium adolescentis exhibits good acid and bile salt tolerance, enabling it to survive and function stably in the intestinal environment.

[0005] Studies have shown that the gut microbiota composition of IBD patients differs significantly from that of healthy individuals, with a marked reduction in Bifidobacterium adolescentis levels. This change may be closely related to the pathogenesis and progression of IBD. The decrease in Bifidobacterium adolescentis may lead to impaired intestinal barrier function, promoting the growth of harmful bacteria and the development of inflammation. Through multiple mechanisms, including improving intestinal barrier function, regulating immune responses, and remodeling the gut microbiota, Bifidobacterium adolescentis holds promise as a new and effective treatment option for IBD patients. Technical issues

[0006] The purpose of this invention is to overcome the shortcomings of the prior art and provide a Bifidobacterium adolescentis strain ibiome027 and its application in inflammatory lesions of the colon. Technical solutions

[0007] This invention is achieved through the following technical solution:

[0008] This invention protects Bifidobacterium adolescentis ibiome027, which is deposited at the China Center for Type Culture Collection (CCTCC), located at Wuhan University, Bayi Road, Wuchang District, Wuhan City, Hubei Province, on December 12, 2024, with accession number CCTCC NO: M 20242783.

[0009] The present invention also protects a drug comprising the above-mentioned Bifidobacterium adolescentis ibiome027 and pharmaceutically acceptable excipients.

[0010] Excipients in pharmaceutical preparations can be classified in various ways, including by source, function and use, and route of administration. Based on source, they can be divided into natural products, semi-synthetic products, and fully synthetic products. Based on their function and use in pharmaceutical preparations, there are 65 categories of excipients, including pH adjusters, chelating agents, inclusion agents, coating agents, protectants, humectants, disintegrants, surfactants, virus inactivators, supplements, precipitants, film-forming materials, flavoring agents, excipients for lyophilization, carbon dioxide adsorbents, foaming agents, aromatics, preservatives, excipients, desiccants, curing agents, buffers, controlled-release materials, adhesives, flavoring agents, antioxidants, antioxidant synergists, anti-adhesion agents, and air displacement agents. Condensing agents, ointment bases, gel materials, polishing agents, propellants, solvents, softeners, emulsifiers, ointment bases, soft capsule materials, lubricants, wetting agents, penetration enhancers, osmotic pressure regulators, suppository bases, sweeteners, fillers, pellet cores, stabilizers, adsorbents, absorbents, diluents, defoamers, flocculants, ethanol modifiers, plaster bases, inks, thickeners, solubilizers, plasticizers, adhesives, excipients for processing traditional Chinese medicine, filter aids, solubilizers, suspending agents, and colorants.

[0011] The pharmaceutically acceptable excipients include at least one of adjuvants, stabilizers or protectants, antibacterial agents, excipients, solubilizers, flavoring agents, diluents, and buffers.

[0012] Adjuvants: Substances that bind to a vaccine antigen to enhance (e.g., strengthen, accelerate, prolong, and / or possibly target) its specific immune response and the clinical efficacy of the vaccine. Stabilizers or Protectants: Substances used to stabilize or protect the active ingredient of a biological product, preventing its degradation or loss of activity. Antimicrobial Agents: Substances used to inhibit microbial growth and prevent microbial contamination. Excipients: Substances used in lyophilized products to shape the drug and act as a scaffold. Solubilizers: Substances used to increase the solubility of a drug. Flavoring Agents: Substances used to improve the taste of oral medications. Diluents and Buffers: Solvents used to dissolve or dilute products and adjust their pH, such as water for injection, sodium chloride injection, and phosphate-buffered saline (PBS).

[0013] Exemplary excipients include, but are not limited to: butylated hydroxytoluene (BHT), calcium carbonate, calcium phosphate (monohydrogen), calcium stearate, croscarmellose, croscarmellose, citric acid, croscarmellose, cysteine, ethyl cellulose, gelatin, hydroxypropyl cellulose, hydroxypropyl methylcellulose, lactose, magnesium stearate, maltitol, mannitol, methionine, methylcellulose, methylparaben, microcrystalline cellulose, polyethylene glycol, povidone, pregelatinized starch, propylparaben, retinyl palmitate, shellac, silica, sodium carboxymethyl cellulose, sodium citrate, sodium glycolate starch, sorbitol, starch (corn), stearic acid, sucrose, talc, titanium dioxide, vitamin A, vitamin E, vitamin C, and xylitol.

[0014] The drug is any one of the following: powder, suspension, granule, capsule, tablet, pill, oral liquid, injection, or powder for injection.

[0015] The drug may be prepared in the form of an injectable formulation or an oral formulation. The injectable formulations are classified according to their physical state as liquid injections, injectable powders, and injectable tablets; and according to the injection site as intradermal injections, subcutaneous injections, intramuscular injections, intravenous injections, and spinal injections; preferably, the solvent for the injectable formulation includes water for injection or physiological saline.

[0016] Orally administered formulations include tablets containing an active ingredient mixed with non-toxic, pharmaceutically acceptable excipients. These excipients may be, for example, inert diluents or fillers (e.g., sucrose, sorbitol, sugar, mannitol, microcrystalline cellulose, starch including potato starch, calcium carbonate, sodium chloride, lactose, calcium phosphate, calcium sulfate, or sodium phosphate); granulators and disintegrants (e.g., cellulose derivatives including microcrystalline cellulose, starch including potato starch, croscarmellose sodium, alginate, or alginic acid); binders (e.g., sucrose, glucose, sorbitol, gum arabic, alginate, sodium alginate, gelatin, starch, pregelatinized starch, microcrystalline cellulose, magnesium aluminum silicate, sodium carboxymethyl cellulose, methylcellulose, hydroxypropyl methylcellulose, ethylcellulose, polyvinylpyrrolidone, or polyethylene glycol); and lubricants, flow aids, and anti-adhesives (e.g., magnesium stearate, zinc stearate, stearic acid, silica, hydrogenated vegetable oil, or talc). Formulations for oral use may also be in the form of chewable tablets or hard gelatin capsules, wherein the active ingredient is mixed with an inert solid diluent (e.g., potato starch, lactose, microcrystalline cellulose, calcium carbonate, calcium phosphate, or kaolin), or in the form of soft gelatin capsules, wherein the active ingredient is mixed with an aqueous or oil medium (e.g., peanut oil, liquid paraffin, or olive oil). Powders, granules, and pills may be prepared using the ingredients mentioned above under tablets or capsules in a conventional manner using, for example, mixers, fluidized bed equipment, or spray drying equipment.

[0017] Other pharmaceutically acceptable excipients for oral formulations include, but are not limited to, colorants, flavoring agents, plasticizers, humectants, and buffers. Formulations for oral use may also be in the form of chewable tablets, or hard gelatin capsules in which the active ingredient is mixed with an inert solid diluent (e.g., potato starch, lactose, microcrystalline cellulose, calcium carbonate, calcium phosphate, or kaolin), or soft gelatin capsules in which the active ingredient is mixed with an aqueous or oil medium (e.g., peanut oil, liquid paraffin, or olive oil). Powders, granules, and pills may be prepared using the ingredients mentioned above under tablets or capsules in a conventional manner using, for example, mixers, fluidized bed equipment, or spray drying equipment.

[0018] In some embodiments, administration of the drugs described herein includes intramuscular, intravenous (e.g., in the form of a sterile solution and in a solvent system suitable for intravenous use), intradermal, intraarticular, intraperitoneal, intralesional, intracranial, intra-articular, intraprostatic, intrapleural, intratracheal, intranasal, intravitreal, intravaginal, intrarectal, transsurface, intratumoral, transperitoneal, subcutaneous, subconjunctival, intracystic, transmucosal, intraperitoneal, intraperitoneal, intraumbilical, intraocular, oral (e.g., tablets, capsules, capsule tablets, capsule-shaped tablets, or syrup), transsurface (e.g., in the form of cream, gel, lotion, or ointment), local, by inhalation, by injection, or by infusion (e.g., continuous infusion in the form of cream or lipid composition, local perfusion directly soaking target cells, catheterization, irrigation).

[0019] The present invention also protects a pharmaceutical composition comprising the above-mentioned Bifidobacterium adolescentis ibiome027 and a combination drug, wherein the combination drug is another drug that has a synergistic effect with Bifidobacterium adolescentis ibiome027.

[0020] Preferably, the combined drug is other bacterial strains or bacterial combinations, such as Bacillus subtilis dual live bacteria, Bifidobacterium triple live bacteria, Clostridium butyricum and Enterococcus triple live bacteria powder, GUT-103, GUT-108, Bacillus subtilis, bacteriophages, etc.; or chemical drugs, such as aminosalicylic acid preparations (including sulfasalazine and 5-aminosalicylic acid preparations, such as mesalazine), glucocorticoids (including methylprednisolone, prednisolone acetate tablets, dexamethasone tablets, etc.), immunosuppressants. Drugs include: anti-tumor necrosis factor (TNF)-α drugs (including infliximab, adalimumab, golimumab, pecelizumab, and ustekinumab), other biological agents (vedelizumab, omalizumab, etc.); small molecule drugs, such as Janus kinase (JAK) inhibitors (such as tofacitinib, utpatinib, etc.); antibiotics, including ciprofloxacin and metronidazole. Other drugs include antidiarrheal drugs (such as loperamide) and analgesics (such as acetaminophen), vitamins, and supplements.

[0021] The effective dosage of this invention is that Bifidobacterium adolescentis ibiome027 is used as the main active pharmaceutical ingredient, and the total number of live bacteria in the live bacterial preparation is 10. 6 -10 14 CFU.

[0022] The duration of medication should be determined based on the desired effect, including but not limited to 1-3 times daily, 3-7 days per week, and also depending on the specific concentration of the formulation.

[0023] The present invention also protects a fermentation agent, functional microbial agent or nutritional composition comprising the above-mentioned Bifidobacterium adolescentis ibiome027; said nutritional composition is a food, nutritional product, supplement, probiotic or symbiotic.

[0024] The fermentation agent or functional microbial agent includes the bacterial liquid prepared from the aforementioned Bifidobacterium adolescentis ibiome027, or the powder or granules obtained by further processing; the fermentation agent may further contain one or more non-antagonistic microbial agents, a compound microbial agent prepared from one or more of Christensenella, Parabacterium, Akkermansia myxophilus, and Bacteroides polymorpha.

[0025] The effective bacterial concentration and viable count are 10. 6 -10 14 CFU.

[0026] Fermentation agents or functional microbial agents can also be used as functional foods and nutritional products.

[0027] Nutritional compositions, including the aforementioned Bifidobacterium adolescentis ibiome027, as well as foods, nutritional products, supplements, probiotics, or symbiotics.

[0028] The food includes the aforementioned Bifidobacterium adolescentis ibiome027 and auxiliary substances that enable the food's functions, and may be presented in forms including but not limited to "dietary supplements" and "fermented foods".

[0029] The dietary supplement includes a bacterial solution or powder prepared from the aforementioned Bifidobacterium adolescentis ibiome027, and further processed with the addition of nutrients such as cellulose, vitamins, and minerals.

[0030] The fermented foods include dairy products, soy products, or fruit and vegetable products. The dairy products include milk, sour cream, or cheese. The soy products include soy milk, fermented black beans, or soy sauce. The fruit and vegetable products include products made from cucumbers, carrots, beets, celery, or cabbage.

[0031] The term "probiotics" refers to live microorganisms that, when provided in appropriate amounts, are beneficial to the health of the host organism. The term "commensal bacteria" refers to foods containing a mixture of prebiotics and probiotics. These typically contain probiotic components that promote growth and / or metabolic activity, and generally, probiotic effects in combination with, but not limited to, Bifidobacterium adolescentis ibiome027 with fructooligosaccharides or galactooligosaccharides.

[0032] This invention further protects the use of the above-mentioned Bifidobacterium adolescentis ibiome027, or the drug, or the drug composition thereof, in the preparation of a drug for the prevention, relief, treatment or adjunctive treatment of inflammatory lesions of the colon.

[0033] The inflammatory lesions of the colon include specific colitis and nonspecific colitis; the nonspecific colitis includes inflammatory bowel disease, which is Crohn's disease or ulcerative colitis; the inflammatory lesions of the colon are acute or chronic.

[0034] Furthermore, the drug is used for at least one of the following purposes: inhibiting weight loss in mammals; inhibiting colonic shortening in mammals; reducing the number of IL-17A+, INF-γ+, and / or TNF-α+ cells in the lamina propria of the mammalian colon; increasing the expression of the tight junction protein ZO-1 in the mammalian colon; reducing the serum TNF-α content in mammals; reducing the levels of IL-6 and / or TNF-α in the colonic tissue of mammals; reducing the expression of IL-17A in the ileal tissue of mammals; and reducing the number of IL-17A+ cells in the lamina propria of the mammalian ileum. Beneficial effects

[0035] This invention identifies a strain of *Bifidobacterium adolescentis* ibiome027 that plays a role in inflammatory bowel disease, specifically in DSS-induced acute colitis, chronic colitis, TNBS-induced acute colitis, and TNF-α-induced colitis. ΔARE It has shown good efficacy in mice, expanding clinical options for the treatment of inflammatory bowel disease and showing great promise. Biological Preservation

[0036] Bifidobacterium adolescentis ibiome027 is deposited at the China Center for Type Culture Collection (CCTCC), Wuhan University, Bayi Road, Wuchang District, Wuhan, Hubei Province, China. The deposit date is December 12, 2024, and the accession number is CCTCC NO: M 20242783. Attached Figure Description

[0037] Figure 1 shows a single colony photograph of Bifidobacterium adolescentis in Example 2;

[0038] Figure 2 shows the microscopic morphology of the colony of Bifidobacterium adolescentis after Gram staining in Example 2;

[0039] Figure 3 is a diagram of the DSS acute colitis experiment in Example 5;

[0040] Figures 4-6 show the effects of Bifidobacterium adolescentis on body weight, colon length, and cytokines in DSS acute colitis mice in Example 5.

[0041] Figure 7 is a diagram of the TNBS acute colitis experiment in Example 6;

[0042] Figures 8-9 show the effects of Bifidobacterium adolescentis on body weight and colon length in mice with TNBS acute colitis in Example 6.

[0043] Figure 10 is a diagram of the DSS chronic colitis experiment in Example 7;

[0044] Figures 11-12 show the effects of Bifidobacterium adolescentis on body weight and ZO-1 expression in DSS chronic colitis mice in Example 7.

[0045] Figures 13-16 show the effect of Bifidobacterium adolescentis on TNF in Example 8. ΔARE The effect of TNF-α levels in mouse serum, TNF-α and IL-6 levels in ileum tissue, IL-17A expression in ileum tissue, and IL-17A secretion in ileal lamina propria cells. Embodiments of the present invention

[0046] To better understand the present invention, the present invention will be further described below with reference to the embodiments and accompanying drawings. The following embodiments are only illustrative of the present invention and are not intended to limit it. Example 1 Isolation of strains

[0047] Recruit healthy volunteers who have not used antibiotics within the past year. After signing an informed consent form, volunteers will collect 2-5 g of fresh feces, place it in a sample collection tube containing glycerol, shake to homogenize, and then place the processed fecal sample in an ice box. The sample will be delivered to the applicant's laboratory within 24 hours for bacterial isolation.

[0048] ① Fecal sample pretreatment: Take 1 mL of the mixture from the sample collection tube containing glycerol and feces, add it to 9 mL of 1× sterile PBS solution, vortex to mix, and then take 100 µL of the mixture and serially dilute it to 10. -9 Used for flat plate coating.

[0049] ② Take 100 μL of the diluted sample and spread it on GAM medium (Qingdao Haibo Biotechnology, HB8518-1). After the dilution solution on the plate surface is free of obvious water marks, invert the plate and place it in an anaerobic workbench for incubation (temperature: 37℃, humidity: 65%, O2: 0%). Incubate statically for 24~36 h. After single colonies grow, perform multiple streak purifications on the single colonies. Perform 16S rRNA sequencing on the purified strains to determine the taxonomic position of the strains.

[0050] ③ 16S rRNA sequencing: Universal primers for the 16S rRNA gene were used: 27F (SEQ ID NO.5: 5'-AGAGTTTGATCMTGGCTCAG-3') and 1492R (SEQ ID NO.6: 5'-TACGGYTACCTTGTTACGACTT-3'). The amplification system consisted of 25 μL of Primerstar (R045Q; Takara), 2 μL of primer 27F, 2 μL of primer 1492R, 1 μL of liquid bacterial culture, and 20 μL of ddH2O. Amplification conditions were: 98℃ for 10 min; 98℃ for 10 s, 56℃ for 15 s, 72℃ for 30 s, for 30 cycles; 72℃ for 5 min. The amplification system was purified by agarose gel electrophoresis. Construction of 16S rRNA gene fragment cloning vector: The ligation system was prepared according to the manufacturer's instructions: 2 μL 16S rRNA gene (30 ng / μL) and 1 μL pEASY®-Blunt Cloning vector (pEASY®-Blunt Cloning kit, CB101-01, Trans), mixed with 2 μL water; reaction conditions: 25℃, 1 h. The mixture was transformed into competent *E. coli* MC 1061 cells. Transformants were selected using antibiotic screening on Luria-Bertani agar supplemented with ampicillin (100 μg / mL, A8108, Solarbio), and plasmids with appropriately sized insert fragments were checked by PCR amplification using primers M13F (SEQ ID NO.7: 5'-TGT AAA ACG ACG GCC AGT-3') and M13R (SEQ ID NO.8: 5'-CAG GAA ACA GCT ATG ACC-3'). Clones containing the putative 16S rRNA gene fragment were randomly selected, from which plasmids were extracted and submitted for insertion sequencing. Agencourt Bioscience Corporation used primers M13F and M13R to perform Sanger sequencing on both strands of the plasmid corresponding to each selected clone. Sequence data were assembled using DNASTAR software (version 5.05 DNAstar, Madison, WI, USA).At least four 16S rRNA sequences, as shown in SEQ ID NO. 1–4, were obtained from a certain strain. Differences were observed near bases 176–195, 203–208, and 1239–1248, confirming that the 16S rRNA gene in this prokaryotic genome is a multiple copy (Yan Yongwei, Zhang Demin. Multiple copies of prokaryotic 16S rRNA genes and their sequence differentiation, Journal of Biology, Vol. 30, No. 4, August 2013, pp. 63–66). Comparison of SEQ ID NO. 1–4 with those in NCBI revealed the strain with the highest similarity to *Bifidobacterium adolescentis* JCM 15918 strain Eg1, therefore this strain belongs to *Bifidobacterium adolescentis*. Example 2 Identification of the strain

[0051] 1. Photograph of a single colony

[0052] The above strains were cultured on GAM medium for 48 hours and photographed. The single colony photo is shown in Figure 1. The colonies are smooth, convex, white, medium-sized, uneven in size, moist, with neat edges, and a diameter of 2.0 mm ± 1 mm.

[0053] 2. Microscopic examination of smears

[0054] The above-mentioned strain was examined under a microscope at 40X, and the microscopic image shown in Figure 2 is obtained. As can be seen from the figure, the strain is Gram-positive, short, curved, club-shaped rod-shaped bacteria.

[0055] 3. Detection of biochemical reactions during sugar alcohol fermentation

[0056] 300 μL of the frozen strain was revived in 1 mL of GAM medium. The liquid cultured strain was purified by streaking on GAM solid medium. A single colony was picked and inoculated into 1 mL of GAM liquid medium and cultured for 24 h. Then, the liquid cultured strain was serially diluted and plated onto GAM solid medium and cultured for 72 h. The biochemical reactions of sugar alcohol fermentation were then detected.

[0057] Single colonies were picked up using a sterilized pipette tip and transferred to a commercially available bacterial biochemical assay ampoule (purchased from Qingdao Haibo Biotechnology). After inoculation, the ampoule was incubated anaerobically at 37°C for 48 hours. The test results were interpreted according to the kit instructions (positive: +; negative: -), as shown in Table 1.

[0058] Table 1 Results of biochemical reaction detection in sugar alcohol fermentation

[0059] Serial Number Name Test Result Serial Number Name Test Result 1 Mannitol Fermentation Tube - 15L - Arabinose + 2D - Ribose + 16 Salicylic Acid + 3 Lactose + 17D - Xylose + 4 Cellobiose - 18D - Sucrose + 5D - Melatonin + 19 Aesculin - 6D - Raffinose + 20 Euonymus - 7 Sorbitol + 21D - Glucose + 8 Starch + 22D - Galactose + 9 Sodium Gluconate - 23 Agonol - 10 Trehalose - 24 Amygdalin + 11 Melibiose + 25D - Fructose + 12 Inositol - 26 Glycogen + 13D - Mannose - 27 Inulin (Inulin Root Powder) + 14D - Maltose + 28 N-Acetylglucosamine -

[0060] The test results confirmed that the strain tested was Bifidobacterium adolescentis.

[0061] The strain was named *Bifidobacterium adolescentis* ibiome027 and deposited at the China Center for Type Culture Collection (CCTCC). The deposit address is: China Center for Type Culture Collection, Wuhan University, Bayi Road, Wuchang District, Wuhan City, Hubei Province, China. The deposit date is December 12, 2024. The accession number is: CCTCC NO: M 20242783. Example 3: Antibiotic susceptibility test of Bifidobacterium adolescentis ibiome027

[0062] Antibiotic susceptibility testing of Bifidobacterium adolescentis was conducted in accordance with the "Technical Requirements for Antimicrobial Susceptibility Testing" (WS / T639-2018), "M100 Antimicrobial Susceptibility Testing Implementation Standard 33rd Edition (Translation)", "Guidelines for Clinical Application of Antimicrobial Drugs", and "M11-A7 Anaerobic Bacterial Drug Susceptibility Testing Method (Approved Standard 7th Edition)".

[0063] According to the aforementioned standards and requirements, ten drugs—ampicillin, imipenem monohydrate, meropenem, clindamycin, piperacillin, tetracycline, moxifloxacin, chloramphenicol, cefoxitin, and cefazolin (purchased from Shanghai Maclean's Biochemical Technology Co., Ltd., Merck Investment (China) Co., Ltd., or Sangon Biotech (Shanghai) Co., Ltd.)—were prepared and serially diluted using the GAM medium for culturing *Bifidobacterium adolescentis*. Eight concentrations were prepared for each drug, and the prepared serially diluted antibacterial solutions were dispensed at 75 μL / well into 96-well microplates. Fresh culture of the *Bifidobacterium adolescentis* strain was serially diluted with GAM medium to a bacterial concentration of approximately 1 × 10⁻⁶. 6Prepare a CFU / mL suspension of the test strain. Add 75 μL of the test strain suspension directly to each antibiotic well. Inoculate wells without antibiotics (75 μL GAM medium plus 75 μL of test strain suspension) as a positive control, and add 150 μL of antibiotic solution (2*maximum detection concentration) to wells without test strain suspension as a negative control. Incubate the inoculated test strain and antibiotic mixture in a 30℃ incubator for 48 h.

[0064] After culture, observe the 96-well plate. The positive control should be turbid; the negative control should be clear and transparent, without contamination. Specific results are shown in Table 2 below, indicating that this strain is sensitive to multiple antibiotics.

[0065] Table 2. Results of antibiotic susceptibility testing of Bifidobacterium adolescentis

[0066] Antibiotic Name Susceptibility Assessment Ampicillin (S), Tetracycline (S), Imipenem (S), Moxifloxacin (S), Meropenem (S), Chloramphenicol (S), Clindamycin (S), Cefoxitin (S), Piperacillin (S), Cefazolin (S), Cefazolin (S)

[0067] Example 4: Bile salt tolerance test of Bifidobacterium adolescentis ibiome027

[0068] 1. Reagent preparation

[0069] (1) Phosphate buffer: Weigh 2.72g of potassium dihydrogen phosphate and dissolve it in 200mL of pure water. Adjust the pH value to 6.8 with sodium hydroxide solution.

[0070] (2) Intestinal fluid: Weigh 0.2 g of bile salts and dissolve them in 20 mL of pure water to prepare 0.1% intestinal fluid.

[0071] 2. Test Methods

[0072] After activation, the bacterial culture was shaken well, and 1 mL was added to 9 mL of buffer or simulated intestinal fluid to obtain samples A (buffer control group) and B (0.1% bile salt simulated intestinal fluid group). After standing, samples were taken at 0 h, 1.5 h, and 3 h. 100 μL of each sample was serially diluted 10-fold to select an appropriate gradient, and 100 μL was spread onto the surface of RCM medium. Each gradient was repeated in triplicate, and the gradient was selected according to the time change. After spreading, the medium was incubated anaerobically at 37 °C, and the colony growth was observed and recorded.

[0073] Select a petri dish with a colony count between 10 and 300, and calculate the viable count using the following formula.

[0074] viable count (CFU / g) = sum of colonies from 3 plates / 3 × 10 × final dilution

[0075] Note: The number of viable bacteria is expressed as "CFU", which stands for bacterial colony unit.

[0076] 3. Experimental Results

[0077] Table 3 Statistical analysis of bile salt tolerance test results

[0078]

[0079] Note: The survival rate is calculated as the ratio of the number of viable bacteria in this group to the number of viable bacteria in the buffer (A) group at 0h.

[0080] As shown in the table above, the survival rate of Bifidobacterium adolescentis in 0.1% bile salt solution is basically the same as that in buffer solution, and it can still remain above 80% after 3 hours, indicating that the strain has good bile salt tolerance. Example 5: Effect of Bifidobacterium adolescentis ibiome027 on acute colitis of DSS

[0081] 1. Experimental Model

[0082] Dextran sulfate sodium (DSS) is a polyanionic derivative of dextran, formed by the esterification reaction of dextran and chlorosulfonic acid. Its molecular formula is (C6H7Na3O). 14 S3) n The molecular weight varies from 36,000 to 50,000, and the sulfur content is generally 17%-20%. Since the first report of using DSS to prepare a hamster ulcerative colitis model in 1985, numerous studies have demonstrated that the DSS colitis model is extremely similar to human ulcerative colitis (UC). The model results show that the experimental animals experience weight loss, diarrhea and bloody stools, intestinal wall thickening, increased infiltrating lymphocytes in the crypts, and severe intestinal tissue damage. The model is simple to establish and operate, inexpensive, reproducible, easy to master and promote, and therefore the most widely used colitis model.

[0083] 2. Experimental Methods

[0084] Eight-week-old C57BL / 6J mice (purchased from Jiangsu Jicui Yaokang Biotechnology Co., Ltd.) were randomly divided into (1) control group: administered 0.2 mL of 0.9% saline by gavage / mouse / day; and (2) experimental group: administered 0.2 mL of 5*10 mice by gavage. 8 CFU / mL Bifidobacterium adolescentis ibiome027 bacterial suspension / bacterium / day (bacterial suspension is prepared by mixing bacterial powder with 0.9% physiological saline).

[0085] The experimental procedure is shown in Figure 3. Mice in the experimental group were treated with Bifidobacterium adolescentis via gavage for one week, while mice in the control group were administered the same volume of physiological saline via gavage. On the first day of modeling (day 8 of the experiment), the C57BL / 6 mice in each group were weighed and marked. The mice's drinking water was replaced with a 2.5% DSS solution, which was changed every three days for seven days. On day 15, the DSS solution was replaced with the mice's normal drinking water. The mice's weight was recorded daily after modeling until the end of the experiment. On day 17 of the experiment, the mice were sacrificed, and colon tissue was collected, photographed, and its length measured.

[0086] After measuring the length of colon tissue, the colon contents were rinsed with PBS, and the intestinal tract was dissected. The intestine was cut into 1-2 cm segments and placed in 10 mL of pre-digestion solution. The mixture was incubated at 37°C and 220 rpm for 20 min. The resulting culture medium was filtered through a 200-mesh steel screen. This process was repeated twice. The remaining tissue was added to a digestion solution containing collagenase and DNase. The filtered result was intestinal lamina propria lymphocytes. The lymphocytes were labeled with specific fluorescent antibodies, and the secretion of INF-γ, IL-17A, and TNF-α was detected by flow cytometry.

[0087] 3. Experimental Results

[0088] (1) Weight

[0089] As shown in Figure 4, the body weight of mice in the control group decreased significantly from day 5 of modeling. Compared with the control group, oral administration of Bifidobacterium adolescentis significantly inhibited the weight loss of mice until the end of the experiment (P<0.01).

[0090] (2) Colon length

[0091] As shown in Figure 5, the average colon length of the control group mice was 5.17 cm, while the average colon length of the mice administered Bifidobacterium adolescentis by gavage was 5.85 cm, which significantly increased the colon length of the DSS acute enteritis mice (P<0.05).

[0092] (3) Secretion of IL-17A, INF-γ and TNF-α

[0093] As shown in Figure 6, mouse colonic lamina propria cells were isolated, and the secretion of IL-17A, INF-γ, and TNF-α was detected. Gavage administration of *Bifidobacterium adolescentis* reduced the number of IL-17A+, INF-γ+, and TNF-α+ cells, with a significant decrease in IL-17A+ cells (P<0.05). IL-17A, IFN-γ, and TNF-α are all pro-inflammatory cytokines. IL-17A can stimulate colonic epithelial cells, fibroblasts, and immune cells, promoting the release of various pro-inflammatory cytokines (such as TNF-α and IL-6) and chemokines (such as CXCL1 and CXCL2), thereby initiating and amplifying the inflammatory response, attracting more immune cells to infiltrate the colonic tissue, and exacerbating inflammatory damage. The reduced number of cells secreting these three pro-inflammatory cytokines indicates a weakened overall inflammatory response. In the state of intestinal inflammation, their reduction demonstrates that *Bifidobacterium adolescentis* alleviates the inflammatory damage to the colonic tissue. Example 6: Effect of Bifidobacterium adolescentis ibiome027 on acute colitis of TNBS

[0094] 1. Experimental Model

[0095] The 2,4,6-trinitrobenzenesulfonic acid (TNBS) colitis model is one of the main models for experimental research on inflammatory bowel disease (IBD) because TNBS-induced inflammation mimics several features of Crohn's disease. TNBS is a small molecule that is not antigenic in itself, but it induces an immune response after binding to host proteins, thus classifying it as a hapten. TNBS treatment in mice can establish a preclinical model of clinical Crohn's disease (CD), characterized by infiltration of CD4+ T cells, neutrophils, and macrophages, leading to transmural inflammation and resulting in transcolonial colitis.

[0096] 2. Experimental Methods

[0097] Eight-week-old C57BL / 6J mice (purchased from Jiangsu Jicui Yaokang Biotechnology Co., Ltd.) were randomly divided into (1) control group: administered 0.2 mL of 0.9% saline by gavage / mouse / day; and (2) experimental group: administered 0.2 mL of 5*10 mice by gavage. 8 CFU / mL Bifidobacterium adolescentis ibiome027 bacterial suspension / bacterium / day (bacterial suspension is prepared by mixing bacterial powder with 0.9% physiological saline).

[0098] The experimental procedure is shown in Figure 7. Mice in the experimental group were treated with Bifidobacterium adolescentis via gavage for one week, while mice in the control group were administered the same volume of physiological saline via gavage. On day 8 of the experiment, 2 cm of tissue was shaved off the backs of the mice. 2The area of ​​fur was covered, and a 1% TNBS solution was applied to the back of the mice, and the mice were weighed. On day 15 of the experiment, 100 μL of a 2.5% TNBS solution was injected into the colon 4 cm from the anus to establish the model. The weight of the mice was recorded daily until the end of the experiment. On day 20 of the experiment, the mice were sacrificed, the colon tissue was collected, photographed, and the length was measured.

[0099] 3. Experimental Results

[0100] (1) Weight

[0101] As shown in Figure 8, the control group mice experienced a sharp decrease in body weight on the first day after modeling, and the weight continued to decrease until the last day; the experimental group mice administered Bifidobacterium adolescentis by gavage experienced a sharp decrease in body weight on the first day after modeling, but their body weight began to recover on the third day and further recovered on the fourth day; and the body weight of the experimental group mice administered Bifidobacterium adolescentis by gavage was significantly different from that of the control group starting from the third day (P < 0.05).

[0102] (2) Colon length

[0103] As shown in Figure 9, the average colon length of mice in the control group was 5.70 cm, while the average colon length of mice in the experimental group that were administered Bifidobacterium adolescentis via gavage was 6.62 cm, which significantly increased the colon length of mice with TNBS acute enteritis (P < 0.05). Example 7: Effect of Bifidobacterium adolescentis ibiome027 on DSS chronic colitis

[0104] 1. Experimental Model

[0105] Chronic colitis can be induced in mice by repeatedly administering low-concentration DSS (e.g., 2%-3%) solution to their drinking water for 5-7 days each time, with a 3-5 day interval between each period of normal water intake, repeated 2-3 times. Mice exhibit fluctuating weight, recurrent diarrhea, chronic inflammation and structural damage to the colon, similar to the course of human chronic colitis, and are often used in the development of long-term treatment drugs for chronic colitis.

[0106] 2. Experimental Methods

[0107] Eight-week-old C57BL / 6J mice (purchased from Jiangsu Jicui Yaokang Biotechnology Co., Ltd.) were randomly divided into (1) control group: administered 0.2 mL of 0.9% saline by gavage / mouse / day; and (2) experimental group: administered 0.2 mL of 5*10 mice by gavage. 8 CFU / mL Bifidobacterium adolescentis ibiome027 bacterial suspension / bacterium / day (bacterial suspension is prepared by mixing bacterial powder with 0.9% physiological saline).

[0108] The experimental procedure is shown in Figure 10. On day 1, the mice's drinking water was replaced with a 2.5% DSS solution, which was changed every three days for 7 days. On day 8, the DSS solution was replaced with normal drinking water for 14 days. On day 22, the mice's drinking water was replaced with a 2.5% DSS solution, which was changed every three days for 7 days. On day 29, the DSS solution was replaced with normal drinking water for 14 days. On day 43, the mice's drinking water was again replaced with a 2.5% DSS solution, which was changed every three days for 7 days. On day 50, the DSS solution was replaced with normal drinking water until the end of the experiment. On day 58, the mice were sacrificed, and colon tissue was collected, photographed, and its length measured.

[0109] 3. Experimental Results

[0110] (1) Weight

[0111] As shown in Figure 11, compared with the control group, the mice in the experimental group that were given Bifidobacterium adolescentis via gavage showed a significant increase in body weight starting from day 32 (the second round of weight recovery in DSS), and the effect continued until the end of the experiment. Furthermore, the weight difference between the mice and the control group increased further during the third round of recovery in DSS (P < 0.05).

[0112] (2) Colonic ZO-1 expression level

[0113] Tight junction protein ZO-1 is a crucial component of tight junctions and an important structural element for maintaining the mechanical barrier and permeability of the mucosal epithelium. Decreased ZO-1 expression not only leads to increased intestinal permeability, but studies have also shown a close relationship between ZO-1 expression and epithelial repair. As shown in Figure 12, gavage administration of Bifidobacterium adolescentis significantly increased ZO-1 expression (P < 0.01), promoting epithelial repair and restoring intestinal wall integrity in colitis mice.

[0114] Example 8: Bifidobacterium adolescentis ibiome027's effect on TNF ΔARE The role of mice

[0115] TNF ΔARE The mouse model is a mutant mouse model that carries a deletion of an AU-rich element (ARE) at the 3'-UTR of the TNFα gene. This deletion enhances the stability of TNFα mRNA and systematically increases the production of its translational products, i.e., systemic TNFα overexpression, which in turn leads to progressive spontaneous arthritis and inflammatory bowel disease.

[0116] 1. Experimental Methods

[0117] 1.1 Experimental Grouping

[0118] Select TNF △ARE Mice (6 weeks old, male) were divided into two groups for the experiment:

[0119] (1) Control group: 0.2 μL of PBS was administered by gavage;

[0120] (2) Experimental group: 10 gavage 8 CFU Bifidobacterium adolescentis ibiome 027.

[0121] Before the experiment, the mice were divided into groups of four. The mice were then weighed. The control group was administered 200 μL of PBS solution by gavage. The experimental group was administered 200 μL of PBS resuspended in 10... 8 CFU. Gavage once a day. For a total of 60 days.

[0122] 1.2 Anatomical sampling

[0123] After the experiment, blood was drawn from the eye socket to obtain serum, and ileum tissue was taken for subsequent testing.

[0124] 1.3 Serum TNF-α detection

[0125] Serum TNF-α levels were detected using a TNF-α enzyme-linked immunosorbent assay kit (elabscience, E-HSEL-M0009).

[0126] 1.4 qPCR of ileal tissue

[0127] (1) Take approximately 2 cm of mouse ileum tissue, add 0.5 mL of Trizol, 0.1 mL of chloroform, and beans, and crush. Centrifuge at 10000 × g for 10 min at 4°C. Transfer the aqueous layer to a new tube, add 0.1 mL of isopropanol, and incubate at room temperature for 10 minutes. Centrifuge at 10000 × g for 10 min at 4°C, and discard the supernatant.

[0128] (2) Add 100 μL of 75% ethanol (prepared with DEPC water) to wash, centrifuge and discard the supernatant (12000 rpm, 4℃, 5 min), centrifuge again and remove the remaining liquid.

[0129] (3) After evaporation for 5-10 min, add DEPC water (about 15-150 μL) according to the size of the precipitate;

[0130] (4) Concentration measurement: Take 2 μL for measurement (set as blank control DEPC);

[0131] (5) DNA removal: Total 8 μL - Calculate template addition amount (μL) based on the detected RNA concentration = 500 / RNA concentration (ng / μL). Add water (addition amount = 6 μL - sample addition amount), add 2 μL of 4 x gDNA Eraser, incubate at 42℃ for 2 min, then maintain at 4℃;

[0132] (6) Reverse transcription: Add 2 μL of 5x reverse transcription reagent to a total volume of 10 μL and perform reverse transcription reaction. The program is as follows: 37℃, 15 min, 85℃, 5 s, 4℃.

[0133] (7) Perform qPCR: Calculate the required mix, each system is 10 μL, containing 5 μL SYBR green, 0.2 μL F, 0.2 μL R, 2 μL template, and 2.6 μL ddH2O. Perform RT-qPCR reaction.

[0134] 1.5 Detection of IL17A in ileal lamina propria cells

[0135] 1.5.1 Isolation of ileal lamina propria cells

[0136] Dissect and collect 2-3 cm of mouse ileum tissue. Rinse the intestinal contents with 1×PBS, remove the Pell's aggregate lymph nodes, remove fat, turn the intestinal segment inside out, and cut it into 0.3-0.5 cm segments into 10 mL of pre-digestion solution. Shake at 37°C and 250 rpm for 20 min. Filter through a steel mesh, collect the intestinal segments, add another 10 mL of pre-digestion solution, and repeat this process three times. After pre-digestion, collect the intestinal segments through a steel mesh, add 10 mL of buffer to wash away residual EDTA, filter through a steel mesh, collect the intestinal segments, add 4 mL of digestion solution, and continue digestion for 30 min. After digestion, vortex to remove impurities, filter through a steel mesh, collect the supernatant, centrifuge at 500 g, 4°C for 5 min, discard the supernatant, add 0.5 mL of buffer, and filter through 200-mesh gauze into 1.5 mL EP tubes. Add 200 µL of cell suspension to a 96-well plate.

[0137] 1.5.2 Pretreatment before flow cytometry detection

[0138] (1) Pretreatment for cell surface molecular detection

[0139] ① Blocking: Centrifuge 500xg external standard plate at 4℃ for 5 min, discard supernatant, add 50uL blocking buffer (containing 0.3uL αCD16 / 32 antibody / well) to each well, mix by pipetting, and react at 4℃ in the dark for 15 min.

[0140] ② Surface molecular staining: Prepare corresponding antibody mixtures with antibody diluent. Add 20 μL of antibody mixture to each well of the sample tube, and add 20 μL of antibody diluent and 0.2 μL of the corresponding single-staining antibody to each well of the single-staining tube. Incubate at 4°C in the dark for 20 min. You can use a pipette to agitate once during the process to avoid uneven staining.

[0141] ③ Termination: After the staining reaction is complete, add 180 μL of antibody diluent to each well, centrifuge at 500 x g for 5 min at 4 °C, discard the supernatant, add 200 μL of antibody diluent to each well, mix by pipetting, and filter through 200 mesh gauze into a flow cytometer for detection.

[0142] (2) Pretreatment for cell surface molecular detection

[0143] ① Blocking: 500xg external standard plate, centrifuged at 4℃ for 5min, discard the supernatant, add 50uL blocking solution to each well, mix by blowing and stirring, and react at 4℃ in the dark for 15min.

[0144] ② Surface molecular staining: Prepare corresponding antibody mixtures with antibody diluent. Add 20 μL of antibody mixture to each well of the sample tube, and add 20 μL of antibody diluent and 0.2 μL of the corresponding single-staining antibody to each well of the single-staining tube. Incubate at 4°C in the dark for 20 min. You can use a pipette to agitate once during the process to avoid uneven staining.

[0145] ③ Termination: After the staining reaction is complete, add 180 μL of antibody diluent to each well, centrifuge at 500 x g for 5 min at 4 °C, discard the supernatant, add 200 μL of antibody diluent to each well, mix by pipetting, and filter through 200 mesh gauze into a flow cytometer for detection.

[0146] 1.6 Detection of inflammatory factors in ileal tissue

[0147] 1.6.1 Extraction of tissue proteins

[0148] (1) Take an appropriate amount of lysis buffer NP40 (Yisheng Bio / 20121ES60, stored at -20℃), and add a final concentration of 1 mM PMSF (stored at -20℃, Yisheng Bio / 20104ES03, stock solution concentration is 200 mM, prepared by weighing 0.3484 g of powder, dissolving it in 10 ml of anhydrous ethanol, and then aliquoting it into 1 ml and freezing it) a few minutes before use. Place it on ice for later use.

[0149] (2) Add 5 steel balls to the pre-cooled lysis buffer at a ratio of 300 μL of lysis buffer per 30 mg of tissue.

[0150] (3) Place the tissue in an EP tube containing 300 EP μL of lysis buffer and steel balls, operate on ice, and shear into small fragments.

[0151] (4) Disrupt cells with ultrasound at 70 Hz for 60 seconds each time, at least 6 times, with a 1-minute interval between each time, and cool on ice. (After homogenization or ultrasound disruption, examine under a microscope. The cell disruption rate should be no less than 90%, and the tissue should be completely lysed without obvious small tissue fragments.)

[0152] (5) Place the centrifuge tubes on ice for 10 minutes to allow for complete lysis.

[0153] (6) After complete lysis, centrifuge at 14,000 g for 5 minutes at low temperature, take the supernatant, and then proceed with subsequent operations such as PAGE, WB and immunoprecipitation.

[0154] (7) Quantify total protein using the BCA protein quantification kit (Yisheng Bio / 20201ES76, BCA Protein Quantification Kit (Enhanced)).

[0155] 1.6.2 Detection of inflammatory factors

[0156] The levels of TNF-α and IL-6 in ileal tissue were detected using an enzyme-linked immunosorbent assay (ELISA) kit.

[0157] 2. Experimental Results

[0158] 2.1 Bifidobacterium adolescentis ibiome027's effect on TNF ΔARE Effect of mouse serum TNF-α levels

[0159] As shown in Figure 13, Bifidobacterium adolescentis ibiome027 can significantly reduce TNF. ΔARE The level of TNF-α in mouse serum (P<0.05).

[0160] 2.2 Bifidobacterium adolescentis ibiome027's effect on TNF ΔARE Effects of inflammatory factors on mouse ileum tissue

[0161] (1) As shown in Figure 14, the levels of protein and inflammatory factors in colon tissue were detected. Bifidobacterium adolescentis ibiome027 could reduce the levels of IL-6 and TNF-α in colon tissue, with IL-6 showing a significant difference (P<0.01).

[0162] (2) As shown in Figure 15, the expression level of the inflammatory factor IL-17A gene in the ileum tissue of mice was detected. Gavage administration of Bifidobacterium adolescentis ibiome 027 can significantly reduce the expression level of the inflammatory factor IL-17A (P<0.05).

[0163] (3) As shown in Figure 16, the lamina propria cells of the mouse ileum were isolated and the secretion of IL-17A was detected. Gavage with Bifidobacterium adolescentis ibiome027 significantly reduced the number of IL-17A+ cells (P<0.05).

[0164] 2.3 Mice that were administered Bifidobacterium adolescentis ibiome027 by gavage showed relief from colitis and arthritis. Example 9 Preparation of bacterial powder containing Bifidobacterium adolescentis

[0165] Bifidobacterium adolescentis ibiome027 (2*10) 9 The bacterial powder containing Bifidobacterium adolescentis (CFU / mL) was anaerobic cultured in GAM medium at 37°C for 24-36 hours, centrifuged, cooled and dried until the moisture content was less than 3%, and then packaged as a fermentation agent, functional bacterial agent or drug.

[0166] Example 10: Solid Beverage Containing Bifidobacterium adolescentis

[0167] A solid beverage containing *Bifidobacterium adolescentis* ibiome027 comprises the following components by weight percentage: 5% dietary fiber powder, 35% stachyose, 30% maltodextrin, and 30% *Bifidobacterium adolescentis* ibiome027. Its preparation method is as follows:

[0168] (1) Preparation of ingredients: Weigh out the dietary fiber powder, stachyose, maltodextrin, and Bifidobacterium adolescentis ibiome027 according to the formula and set aside;

[0169] (2) Initial mixture: Add dietary fiber powder, stachyose and maltodextrin and mix evenly to obtain the initial mixture for later use;

[0170] (3) Secondary mixing: Add Bifidobacterium adolescentis ibiome027 to the primary mixture prepared in step (2) and mix evenly under low temperature;

[0171] (4) Packaging: The mixture from step (3) is packaged to obtain a solid beverage containing Bifidobacterium adolescentis ibiome027. Example 11 Dairy products containing Bifidobacterium adolescentis

[0172] A coagulated fermented dairy product containing Bifidobacterium adolescentis ibiome027 is prepared according to the following steps:

[0173] (1) Weigh 10kg of raw milk, standardize it, add 5g of zinc sulfate and 0.8kg of arabinose, mix evenly and put it into a mixing tank to obtain material 1;

[0174] (2) Homogenize material 1 at 70℃ and 20MPa for 10 min, and sterilize it at 90~95℃ for 5~10 min to obtain material 2;

[0175] (3) Quickly cool material 2 to 35-39°C, inoculate with Bifidobacterium adolescentis ibiome027 at an inoculation rate of 0.01%, fill, cover, and ferment at 37°C until curd forms. When the curd is in good condition and the pH reaches 4.2-4.5, the fermentation is complete. Stop fermentation and quickly place in a refrigerated room at 2-6°C for 12 hours of post-ripening. This yields a coagulated fermented milk (i.e., yogurt) prepared using Bifidobacterium adolescentis ibiome027 as the starter culture. Example 12 Fermented fruit and vegetable products containing Bifidobacterium adolescentis

[0176] A fermented fruit and vegetable product containing Bifidobacterium adolescentis ibiome027 is prepared using the following method:

[0177] (1) Take 5kg of fruit and vegetable raw materials, add 5kg of purified water, 5g of zinc sulfate, and mix evenly with 1.0kg of arabinose to obtain material 3;

[0178] (2) Homogenize material 3 at 70℃ and 20MPa for 10 min, and sterilize it at 90~95℃ for 5~10 min to obtain material 4;

[0179] (3) The material 4 is rapidly cooled to 37°C, and Bifidobacterium adolescentis ibiome027 is inoculated at an inoculation rate of 0.01%. The mixture is then filled, covered, and fermented in a fermentation chamber at 37°C for 16 hours. After fermentation, the mixture is rapidly cooled to 4°C and maintained for about 12 hours to produce fermented fruit and vegetable products prepared using Bifidobacterium adolescentis ibiome027 as a starter culture.

[0180] The above-described embodiments are merely preferred embodiments of the present invention and are not intended to limit the scope of the present invention. Various modifications and improvements made by those skilled in the art to the technical solutions of the present invention without departing from the spirit of the present invention should fall within the protection scope defined by the claims of the present invention.

Claims

1. Bifidobacterium adolescentis ibiome027, characterized by: The Bifidobacterium adolescentis strain is deposited at the China Center for Type Culture Collection (CCTCC), located at Wuhan University, Bayi Road, Wuchang District, Wuhan City, Hubei Province, on December 12, 2024, with accession number CCTCC NO: M 20242783.

2. A drug, characterized in that: It includes Bifidobacterium adolescentis ibiome027 as described in claim 1 and pharmaceutically acceptable excipients; preferably, the pharmaceutically acceptable excipients include at least one of adjuvants, stabilizers or protectants, antibacterial agents, excipients, solubilizers, flavoring agents, diluents, and buffers.

3. A pharmaceutical composition, characterized in that: The invention includes Bifidobacterium adolescentis ibiome027 as described in claim 1 and a combination drug, wherein the combination drug is another drug that has a synergistic effect with Bifidobacterium adolescentis ibiome027.

4. The pharmaceutical composition according to claim 3, characterized in that: The combined drugs are other strains or strain combinations, or chemical drugs, biological agents, small molecule drugs, antibiotics, or other drugs.

5. A fermentation agent, functional microbial agent, or nutritional composition comprising Bifidobacterium adolescentis ibiome027 as described in claim 1.

6. The fermentation agent, functional microbial agent, or nutritional composition containing *Bifidobacterium adolescentis* ibiome027 according to claim 5, characterized in that: The nutritional composition is a food, nutritional product, supplement, probiotic, or symbiotic.

7. The use of Bifidobacterium adolescentis ibiome027 as described in claim 1, or the medicament as described in claim 2, or the pharmaceutical composition as described in any one of claims 3 to 4, in the preparation of a medicament for reducing inflammation in tissues or organs of a subject.

8. The use of Bifidobacterium adolescentis ibiome027 as described in claim 1, or the medicament as described in claim 2, or the pharmaceutical composition as described in any one of claims 3 to 4 in the preparation of a medicament for the prevention, relief, treatment or adjunctive treatment of inflammatory bowel disease.

9. The application according to claim 8, characterized in that: The inflammatory lesions of the colon include specific colitis and nonspecific colitis; the nonspecific colitis includes inflammatory bowel disease, which is Crohn's disease or ulcerative colitis; the inflammatory lesions of the colon are acute or chronic.

10. The application according to any one of claims 7 to 9, characterized in that, The drug is used for at least one of the following purposes: Inhibits weight loss in mammals; Inhibits the shortening of the colon in mammals; It reduces the number of IL-17A+, INF-γ+ and / or TNF-α+ cells in the lamina propria of the mammalian colon. Increase the expression level of the mammalian colonic tight junction protein ZO-1; It reduces the level of TNF-α in mammalian serum; Reduces IL-6 and / or TNF-α levels in mammalian colon tissue; Reduces IL-17A expression in mammalian ileum tissue; It reduces the number of IL-17A+ cells in the lamina propria of the mammalian ileum.

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