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肠道微生物群在胃肠道免疫稳态和炎症中的作用:对炎症性肠病的影响

The Role of Gut Microbiota in Gastrointestinal Immune Homeostasis and Inflammation: Implications for Inflammatory Bowel Disease.

作者信息

Bretto Elisabetta, Urpì-Ferreruela Miquel, Casanova Gherzon Rimer, González-Suárez Begoña

机构信息

Endoscopy Unit, Gastroenterology Department, Hospital Clínic of Barcelona, 08036 Barcelona, Spain.

出版信息

Biomedicines. 2025 Jul 24;13(8):1807. doi: 10.3390/biomedicines13081807.

Abstract

Inflammatory bowel disease (IBD), a heterogeneous group of recurring inflammatory conditions of the digestive system that encompass both ulcerative colitis (UC) and Crohn's disease (CD), pose a significant public health challenge, currently lacking a definitive cure. The specific etiopathogenesis of IBD is not yet fully understood, but a multifactorial interplay of genetic and environmental factors is suspected. A growing body of evidence supports the involvement of intestinal dysbiosis in the development of IBD, including the effects of dysbiosis on the integrity of the intestinal epithelial barrier, modulation of the host immune system, alterations in the enteric nervous system, and the perpetuation of chronic inflammation. A comprehensive understanding of these mechanisms is important to define preventive measures, to develop new effective and lasting treatments, and to improve disease outcome. This review examines the complex tri-directional relationship between gut microbiota, mucosal immune system, and intestinal epithelium in IBD. In addition, nonpharmacological and behavioral strategies aimed at restoring a proper microbial-immune relationship will be suggested.

摘要

炎症性肠病(IBD)是一组异质性的复发性消化系统炎症性疾病,包括溃疡性结肠炎(UC)和克罗恩病(CD),对公共卫生构成重大挑战,目前仍缺乏根治方法。IBD的具体发病机制尚未完全明确,但怀疑是遗传和环境因素的多因素相互作用所致。越来越多的证据支持肠道菌群失调参与了IBD的发生发展,包括菌群失调对肠道上皮屏障完整性的影响、对宿主免疫系统的调节、肠神经系统的改变以及慢性炎症的持续存在。全面了解这些机制对于确定预防措施、开发新的有效持久治疗方法以及改善疾病预后至关重要。本综述探讨了IBD中肠道微生物群、黏膜免疫系统和肠上皮之间复杂的三向关系。此外,还将提出旨在恢复适当微生物-免疫关系的非药物和行为策略。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5f4c/12383986/30f84e6f2412/biomedicines-13-01807-g001.jpg

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