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胆汁酸相关调控黏膜炎症和肠道动力:从发病机制到在 IBD 和显微镜结肠炎中的治疗应用。

Bile Acid-Related Regulation of Mucosal Inflammation and Intestinal Motility: From Pathogenesis to Therapeutic Application in IBD and Microscopic Colitis.

机构信息

IBD Unit-UOS Malattie Infiammatorie Croniche Intestinali, CEMAD, Digestive Diseases Center, Fondazione Policlinico Universitario "A. Gemelli" IRCCS, Università Cattolica del Sacro Cuore, L. Go A. Gemelli 8, 00168 Rome, Italy.

Dipartimento di Medicina e Chirurgia Traslazionale, Università Cattolica del Sacro Cuore, L. Go F. Vito 1, 00168 Rome, Italy.

出版信息

Nutrients. 2022 Jun 27;14(13):2664. doi: 10.3390/nu14132664.

DOI:10.3390/nu14132664
PMID:35807844
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9268369/
Abstract

Inflammatory bowel diseases (IBD) and microscopic colitis are chronic immune-mediated inflammatory disorders that affect the gastroenterological tract and arise from a complex interaction between the host's genetic risk factors, environmental factors, and gut microbiota dysbiosis. The precise mechanistic pathways interlinking the intestinal mucosa homeostasis, the immunological tolerance, and the gut microbiota are still crucial topics for research. We decided to deeply analyze the role of bile acids in these complex interactions and their metabolism in the modulation of gut microbiota, and thus intestinal mucosa inflammation. Recent metabolomics studies revealed a significant defect in bile acid metabolism in IBD patients, with an increase in primary bile acids and a reduction in secondary bile acids. In this review, we explore the evidence linking bile acid metabolites with the immunological pathways involved in IBD pathogenesis, including apoptosis and inflammasome activation. Furthermore, we summarize the principal etiopathogenetic mechanisms of different types of bile acid-induced diarrhea (BAD) and its main novel diagnostic approaches. Finally, we discuss the role of bile acid in current and possible future state-of-the-art therapeutic strategies for both IBD and BAD.

摘要

炎症性肠病(IBD)和显微镜下结肠炎是慢性免疫介导的炎症性疾病,影响胃肠道,源于宿主遗传风险因素、环境因素和肠道微生物失调之间的复杂相互作用。将肠道黏膜稳态、免疫耐受和肠道微生物群联系起来的确切机制途径仍然是研究的关键主题。我们决定深入分析胆汁酸在这些复杂相互作用中的作用及其在调节肠道微生物群和肠道黏膜炎症中的代谢作用。最近的代谢组学研究揭示了 IBD 患者胆汁酸代谢的显著缺陷,初级胆汁酸增加,次级胆汁酸减少。在这篇综述中,我们探讨了将胆汁酸代谢物与涉及 IBD 发病机制的免疫途径联系起来的证据,包括细胞凋亡和炎性体激活。此外,我们总结了不同类型胆汁酸诱导腹泻(BAD)的主要发病机制及其主要的新诊断方法。最后,我们讨论了胆汁酸在 IBD 和 BAD 的当前和未来最先进治疗策略中的作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/66f5/9268369/fa826fa220dd/nutrients-14-02664-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/66f5/9268369/9ae74ac23b3d/nutrients-14-02664-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/66f5/9268369/fa826fa220dd/nutrients-14-02664-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/66f5/9268369/9ae74ac23b3d/nutrients-14-02664-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/66f5/9268369/fa826fa220dd/nutrients-14-02664-g002.jpg

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