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REVIEW article

Front. Immunol.

Sec. Mucosal Immunity

This article is part of the Research TopicHost-Microbiota Interactions in IBD: Immune Modulation and Barrier FunctionView all 4 articles

The Gut Microbiota and its Metabolites: Novel Therapeutic Targets for Inflammatory Bowel Disease

Provisionally accepted
  • Affiliated Hospital of Jiangsu University, Zhenjiang, China

The final, formatted version of the article will be published soon.

Inflammatory bowel disease (IBD) pathogenesis is critically influenced by gut microbiota dysbiosis and perturbations in associated metabolites. This review outlines current IBD diagnostic and therapeutic paradigms, highlighting the persistent focus on the management of inflammatory symptoms and the absence of curative interventions. We elucidate the mechanistic links between gut microbiota dysregulation and IBD progression, with an emphasis on the immunomodulatory functions of microbial metabolites—specifically short-chain fatty acids (SCFAs), bile acids (BAs), and tryptophan (Trp) metabolism—in maintaining intestinal barrier integrity and attenuating inflammation. Furthermore, we evaluate microbiota-targeted therapeutic strategies, including probiotics, fecal microbiota transplantation (FMT), and metabolite-based interventions, as novel approaches for IBD management. This synthesis aims to inform future therapeutic development and accelerate the clinical translation of microbiota-modulating regimens.

Keywords: inflammatory bowel disease, Gut Microbiota, short-chain fatty acids, Bile acids, Tryptophan

Received: 28 Aug 2025; Accepted: 10 Nov 2025.

Copyright: © 2025 Shen, Li, Wang and Sun. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

* Correspondence:
Deqiang Wang, deqiang_wang@aliyun.com
Kang Sun, doctorsunkang@126.com

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