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Association between intestinal microbiota and inflammatory bowel disease

期刊

ANIMAL MODELS AND EXPERIMENTAL MEDICINE
卷 5, 期 4, 页码 311-322

出版社

WILEY
DOI: 10.1002/ame2.12255

关键词

dysbiosis; IBD model; intestinal microbiota; metabolites

资金

  1. Higher Education Discipline Innovation Project [B16044]
  2. National Natural Science Foundation of China [31625025, 32000082]
  3. R&D Program of Beijing Municipal Education Commission [KM202212448002]

向作者/读者索取更多资源

Inflammatory bowel disease (IBD) is a global disease with high incidence, long duration, and low curability. Dysbiosis of intestinal microbiota is widely recognized as a pathology of IBD, but its precise role in the disease process is still unclear. This review outlines the relationship between intestinal microbiota and IBD, and their contribution to the pathogenesis of the disease through dysregulated metabolite production.
Inflammatory bowel disease (IBD), which includes Crohn's disease (CD) and ulcerative colitis (UC), has emerged as a global disease with high incidence, long duration, devastating clinical symptoms, and low curability (relapsing immune response and barrier function defects). Mounting studies have been performed to investigate its pathogenesis to provide an ever-expanding arsenal of therapeutic options, while the precise etiology of IBD is not completely understood yet. Recent advances in high-throughput sequencing methods and animal models have provided new insights into the association between intestinal microbiota and IBD. In general, dysbiosis characterized by an imbalanced microbiota has been widely recognized as a pathology of IBD. However, intestinal microbiota alterations represent the cause or result of IBD process remains unclear. Therefore, more evidences are needed to identify the precise role of intestinal microbiota in the pathogenesis of IBD. Herein, this review aims to outline the current knowledge of commonly used, chemically induced, and infectious mouse models, gut microbiota alteration and how it contributes to IBD, and dysregulated metabolite production links to IBD pathogenesis.

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