ArticleFrontiers in microbiology2025
Gut microbiota and their metabolites ameliorate acute and chronic colitis in mice via modulating Th17/Treg balance.
Article in Frontiers in microbiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Gut-kidney axis: Dysbiosis and renal disease.World journal of nephrology · 2026Review
- Fecal microbiota transplantation in ulcerative colitis: mucosal immune mechanisms and precision microbiota therapy.Frontiers in immunology · 2026Review
- Fecal microbiota transplantation alleviates DSS-induced colitis: increased fecal butyrate, reduced colonic p65 phosphorylation, and altered Th17/Treg ratios in the spleen and mesenteric lymph nodes.Frontiers in immunology · 2026Article
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Authors and funding
8 authors.
Funding
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Abstract
Introduction: Ulcerative colitis (UC) is a recurrent inflammatory bowel disease affecting the colorectum, which remains a prominent research focus due to significant individual variations in clinical therapeutic outcomes. Fecal microbiota transplantation (FMT), as a therapeutic approach to restore intestinal homeostasis, has demonstrated favorable efficacy in UC management. However, given the characteristic alternating cycles of active and remission phases in UC, there remains a paucity of in-depth research regarding the optimal timing for FMT intervention. Concurrently, butyrate - a crucial microbial metabolite - ameliorates murine colitis through both direct and indirect mechanisms, while the therapeutic effectiveness of FMT in UC correlates closely with intestinal butyrate concentration. Methods: This study established acute and chronic UC murine models and employed FMT and butyrate interventions to monitor dynamic alterations in gut microbiota and lymphocyte subsets. Through comprehensive analyses, we aimed to elucidate the interplay between gut microbiota and host immune mechanisms, identify the optimal therapeutic timing for UC interventions, and evaluate the mechanistic role of butyrate. These findings provide theoretical foundations for personalized microbiota-targeted therapies in UC. Results: Our findings demonstrate that gut microbiota and their metabolites exert therapeutic effects on murine acute/chronic colitis through modulation of the T helper cell 17 (Th17)/T regulatory cell (Treg) ratio. Specifically, the remission phase represents a more favorable window for intestinal homeostasis modulation, with combination therapy involving microbial metabolites exhibiting superior anti-inflammatory efficacy. Discussion: The maintenance of an appropriate Th17/Treg equilibrium during microbiota restoration demonstrates therapeutic advantages. Notably, butyrate synergistically enhances microbial therapeutic effects, providing experimental evidence for personalized modulation of gut ecosystems in inflammatory bowel disease management.
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