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Furthermore, such variation has been associated with differing inter\u2010individual susceptibility to the development of inflammatory bowel disease (IBD), a chronic inflammatory disease of the gastrointestinal tract that is driven by dysfunctional immune\u2010microbiome interactions. Here, we identified that differences in microbiome composition in C57BL\/6 mice from two commonly used commercial vendors, Charles River (CR) and Jackson (JAX) Laboratories, were associated with variation in the intestinal immune phenotype, with CR mice having greater Th17 levels and faecal IgA. In turn, CR mice demonstrated enhanced susceptibility to the dextran sulfate sodium (DSS)\u2010induced model of colitis compared to JAX mice. Co\u2010housing studies revealed that CR mice could transmit enhanced susceptibility to colitis to JAX mice, implicating differences in microbiome composition as drivers of disease susceptibility. Faecal metabolomics studies using targeted mass spectrometry revealed several metabolites differentially enriched in colitis\u2010susceptible and colitis\u2010resistant mice. Correlation analysis uncovered metabolites that were both negatively and positively associated with colitis severity. Taken together, our study leveraged natural microbiome variation to identify gut microbial metabolites with the potential to predict the severity of IBD. Importantly, we further establish susceptible and non\u2010susceptible murine microbial communities that represent a tractable system in which to further uncover microbiome contributions to IBD in the DSS\u2010colitis model.<\/jats:p>","DOI":"10.1111\/imm.70071","type":"journal-article","created":{"date-parts":[[2025,12,10]],"date-time":"2025-12-10T02:10:53Z","timestamp":1765332653000},"page":"766-783","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Variation in Microbiome Composition and Faecal Metabolites Are Associated With Differential Susceptibility to\n                    <scp>DSS<\/scp>\n                    \u2010Induced Colitis"],"prefix":"10.1111","volume":"177","author":[{"given":"Jessica M.","family":"Till","sequence":"first","affiliation":[{"name":"Department of Cardiovascular and Metabolic Sciences Cleveland Clinic Research, Cleveland Clinic  Cleveland Ohio USA"},{"name":"Center for Microbiome and Human Health Cleveland Clinic Research, Cleveland Clinic  Cleveland Ohio USA"},{"name":"Department of Molecular Medicine Cleveland Clinic Lerner College of Medicine, Case Western Reserve University  Cleveland Ohio USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Orion D.","family":"Brock","sequence":"additional","affiliation":[{"name":"Department of Cardiovascular and Metabolic Sciences Cleveland Clinic Research, Cleveland Clinic  Cleveland Ohio USA"},{"name":"Center for Microbiome and Human Health Cleveland Clinic Research, Cleveland Clinic  Cleveland Ohio USA"},{"name":"Department of Molecular Medicine Cleveland Clinic Lerner College of Medicine, Case Western Reserve University  Cleveland Ohio USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-3264-8138","authenticated-orcid":false,"given":"Elyza A.","family":"Do","sequence":"additional","affiliation":[{"name":"Department of Microbiology &amp; Plant Pathology University of California Riverside  Riverside California USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Morgan J.","family":"Engelhart","sequence":"additional","affiliation":[{"name":"Department of Cardiovascular and Metabolic Sciences Cleveland Clinic Research, Cleveland Clinic  Cleveland Ohio USA"},{"name":"Center for Microbiome and Human Health Cleveland Clinic Research, Cleveland Clinic  Cleveland Ohio USA"},{"name":"Department of Molecular Medicine Cleveland Clinic Lerner College of Medicine, Case Western Reserve University  Cleveland Ohio USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Robert W. 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