Inflammatory bowel disease is not exclusively a human affliction. Dogs, cats, and livestock all suffer from chronic colitis-like syndromes marked by persistent diarrhoea, weight loss, abdominal discomfort, and impaired nutrient absorption. In veterinary clinics, these conditions are typically managed with corticosteroids, antibiotics, and immunomodulators, yet treatment failures and side effects are common enough that researchers have been searching for safer alternatives. Now, a new experimental study published in Veterinary Medicine and Science offers compelling evidence that two well-known probiotic bacteria, Bacillus coagulans and Lactobacillus acidophilus, can significantly reduce intestinal inflammation in an animal model of ulcerative colitis, and that their benefit may stem from a surprising molecular target: the NLRP3 inflammasome.
The research team, led by Fatemeh Shayesteh and colleagues at Shahrekord University of Medical Sciences in Iran, set out to test whether these two probiotic strains could modulate inflammasome signalling, a pathway increasingly implicated in chronic mucosal inflammation across species. Inflammasomes are cytosolic protein complexes that act as intracellular alarm systems, sensing microbial or endogenous danger signals and activating the enzyme caspase-1. Once activated, caspase-1 cleaves and matures the potent inflammatory cytokines interleukin-1β and interleukin-18, which drive neutrophil recruitment, tissue damage, and the self-perpetuating cycle of inflammation characteristic of colitis. When the NLRP3 inflammasome becomes overactive, as has been documented in both human and veterinary cases of inflammatory bowel disease, the result is persistent mucosal injury and poor healing.
To model the disease, the researchers induced ulcerative colitis in 40 male Wistar rats by administering a single intrarectal dose of 4% acetic acid under anaesthesia, a well-established chemical method that reproduces key histopathological features seen in naturally occurring colitis of dogs, cats, and cattle, including mucosal ulceration, epithelial barrier dysfunction, and infiltration of inflammatory cells. The animals were randomly divided into five groups of eight: a healthy control group receiving saline, an untreated colitis group, a group treated with the standard anti-inflammatory drug mesalazine at 300 mg/kg per day, and two probiotic groups receiving daily oral gavage of either B. coagulans or L. acidophilus at a concentration of 10⁹ colony-forming units per millilitre for seven consecutive days. On day ten, the rats were euthanized and colonic tissues were collected for molecular, biochemical, and histological analysis.
The molecular results were striking. Compared with healthy controls, colitis induction caused dramatic upregulation of inflammasome-related genes in colonic tissue: interleukin-18 expression rose roughly 7.6-fold, NLRP3 about 11-fold, caspase-1 more than 12-fold, and tumour necrosis factor-alpha more than 6-fold. Treatment with either probiotic strain significantly reversed these changes. In the L. acidophilus group, expression of all four genes fell substantially relative to untreated colitis animals, and B. coagulans produced reductions of similar magnitude. Notably, the probiotic effects were comparable to those achieved with mesalazine, the benchmark therapy, which itself suppressed the same gene set. The convergence of probiotic and pharmacological outcomes at the transcript level suggests that these bacteria engage the same inflammatory circuitry that conventional drugs target, but through biological mechanisms rather than chemical inhibition.
Protein-level measurements reinforced the gene expression data. Using enzyme-linked immunosorbent assays on colonic tissue homogenates, the team found that colitis induction caused enormous increases in interleukin-1β and interleukin-17 protein concentrations. Both probiotics significantly lowered these cytokines, again paralleling the effect of mesalazine. Interleukin-1β is the direct downstream product of caspase-1 activation within the inflammasome, so its reduction provides functional confirmation that probiotic treatment genuinely dampens inflammasome output rather than merely altering gene transcription. Interleukin-17, meanwhile, is a signature cytokine of the Th17 immune axis that drives neutrophil recruitment and barrier disruption, meaning the probiotics appeared to suppress inflammation at multiple points along the pathological cascade.
The structural evidence was equally persuasive. Macroscopic examination of the colons, scored independently by two blinded observers using the Wallace and Keenan system, revealed severe ulceration, hyperaemia, inflammation, and oedema in untreated colitis animals, with a mean wound score of 3.25. Both probiotic groups showed marked improvement, with L. acidophilus achieving a mean score of 1.50, identical to the mesalazine group, and B. coagulans scoring 1.83. Colon length and weight, which serve as indirect measures of tissue oedema and shortening, were significantly restored in both probiotic groups compared with the untreated colitis group, indicating that the bacteria helped preserve gross tissue morphology.
Under the microscope, the differences were just as clear. Haematoxylin and eosin stained sections from untreated colitis rats displayed pronounced thickening of the mucosal, submucosal, and muscularis layers, extensive epithelial cell loss, a marked reduction in goblet cells, severe leukocyte infiltration, and lymphoid hyperplasia across all tissue layers. In contrast, sections from probiotic-treated animals showed reduced layer thickness, fewer inflammatory cells, milder crypt damage, and tissue involvement confined to the 1 to 25% range, compared with 51 to 75% in the colitis group. Histopathological scores fell from 4 in the colitis group to 2 in both probiotic groups, matching the mesalazine-treated animals. The restoration of goblet cells, which produce the protective mucus layer lining the gut, points to genuine epithelial repair rather than simple suppression of visible inflammation.
The mechanistic story behind these findings is likely multifaceted. Probiotics are known to reinforce epithelial integrity, compete with pathogenic bacteria for adhesion sites and nutrients, produce antimicrobial compounds, and regulate immune cell activity through Toll-like receptor pathways and the production of short-chain fatty acids. The authors suggest that suppression of inflammasome signalling may occur indirectly through these routes: by modulating Toll-like receptor activation, probiotics can shift the danger-sensing environment of the gut mucosa away from the chronic alarm state that keeps NLRP3 primed. Each strain also brings distinct practical advantages. B. coagulans is a spore-forming lactic acid bacterium whose resilient spores survive harsh storage conditions and the acidic gauntlet of the gastrointestinal tract, a trait particularly valuable in farm settings. L. acidophilus, by contrast, is a strong colonizer of the intestinal tract with well-documented immunomodulatory properties, making it well suited to companion animals with chronic enteropathies.
The veterinary implications extend well beyond the laboratory. Chronic inflammatory gut diseases reduce productivity in livestock, impair growth in young animals, and increase morbidity in pets, while long-term drug therapy raises concerns about cost, side effects, and, in food animals, drug residues in the food supply. Probiotics that measurably reduce inflammasome activation and pro-inflammatory cytokines could serve as adjuncts that allow lower doses of conventional drugs, or as standalone interventions in milder cases. The study also fits into a broader trend in veterinary microbiology toward multi-strain formulations, since combinations of Bacillus and Lactobacillus species are thought to target different aspects of gut ecology and immune regulation simultaneously, potentially offering synergistic benefits over single-strain products.
Important caveats remain. Some inflammation and leukocyte infiltration persisted even in probiotic-treated animals, indicating that these bacteria alleviate disease severity but may not fully replace pharmacological therapy in severe cases. Moreover, the murine model, while translational, differs from dogs, cats, and livestock in microbiota composition and immune function, so clinical trials in target veterinary species are the necessary next step, along with optimization of dosing regimens and formulation of multi-strain products tailored to different animal populations. Still, by connecting a practical, shelf-stable probiotic pair to a specific molecular pathway central to colitis pathology, the study provides a mechanistic bridge between the empirical use of probiotics in animal health and the modern immunology of inflammatory disease, and it does so with the kind of rigorous, multi-level evidence, from gene expression to protein to tissue architecture, that could finally move veterinary probiotics from folklore to pharmacology.
Subject of Research: Probiotic modulation of NLRP3 inflammasome signalling in experimental ulcerative colitis
Article Title: Probiotic Intervention With Bacillus coagulans and Lactobacillus acidophilus in Small Animals Experimental Ulcerative Colitis: Insights From a Small Animal Model
Article References: Shayesteh, F., Shahini Shams Abadi, M., Rouhi, L., Doosti, A., & Bagheri, N. (2026). Probiotic Intervention With Bacillus coagulans and Lactobacillus acidophilus in Small Animals Experimental Ulcerative Colitis: Insights From a Small Animal Model. Veterinary Medicine and Science, 12(6), Article e70883. https://doi.org/10.1002/vms3.70883
Image Credits: AI Generated
DOI: 10.1002/vms3.70883
Keywords: probiotics, Bacillus coagulans, Lactobacillus acidophilus, ulcerative colitis, NLRP3 inflammasome, veterinary medicine, inflammatory bowel disease, interleukin-1beta, mesalazine, rat model, gut microbiota, cytokines
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William Thompson. (October 1, 2026). Two Probiotic Strains Calm Gut Inflammation by Taming the NLRP3 Inflammasome. Scienmag. https://scienmag.com/two-probiotic-strains-calm-gut-inflammation-by-taming-the-nlrp3-inflammasome/
William Thompson. “Two Probiotic Strains Calm Gut Inflammation by Taming the NLRP3 Inflammasome.” Scienmag, 1 October 2026, https://scienmag.com/two-probiotic-strains-calm-gut-inflammation-by-taming-the-nlrp3-inflammasome/. Accessed 1 October 2026.
William Thompson. “Two Probiotic Strains Calm Gut Inflammation by Taming the NLRP3 Inflammasome.” Scienmag. October 1, 2026. https://scienmag.com/two-probiotic-strains-calm-gut-inflammation-by-taming-the-nlrp3-inflammasome/
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Tags: animal models of ulcerative colitisBacillus coagulansBacillus coagulans and Lactobacillus acidophilus in gut healthchronic mucosal inflammation in veterinary medicinecytokine regulation in gut inflammationcytokinesgastrointestinal health in dogs and livestockgut microbiotaimmune response modulation by probioticsinflammasinflammatory bowel diseaseinterleukin-1betaLactobacillus acidophilusmesalazinemolecular mechanisms of probiotic actionNLRP3 inflammasomeNLRP3 inflammasome role in inflammatory bowel diseaseprobiotic bacteria for intestinal inflammationprobioticsprobiotics as alternative therapy for colitisrat modelsafety and side effects of conventional colitis treatmentsulcerative colitisVeterinary Medicine
