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肠道微生物群与免疫系统的相互作用

Gut Microbiota and Immune System Interactions.

作者信息

Yoo Ji Youn, Groer Maureen, Dutra Samia Valeria Ozorio, Sarkar Anujit, McSkimming Daniel Ian

机构信息

College of Nursing, University of South Florida, Tampa, FL 33612, USA.

College of Nursing, University of Tennessee-Knoxville, Knoxville, TN 37916, USA.

出版信息

Microorganisms. 2020 Oct 15;8(10):1587. doi: 10.3390/microorganisms8101587.

DOI:10.3390/microorganisms8101587
PMID:33076307
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7602490/
Abstract

Dynamic interactions between gut microbiota and a host's innate and adaptive immune systems play key roles in maintaining intestinal homeostasis and inhibiting inflammation. The gut microbiota metabolizes proteins and complex carbohydrates, synthesize vitamins, and produce an enormous number of metabolic products that can mediate cross-talk between gut epithelial and immune cells. As a defense mechanism, gut epithelial cells produce a mucosal barrier to segregate microbiota from host immune cells and reduce intestinal permeability. An impaired interaction between gut microbiota and the mucosal immune system can lead to an increased abundance of potentially pathogenic gram-negative bacteria and their associated metabolic changes, disrupting the epithelial barrier and increasing susceptibility to infections. Gut dysbiosis, or negative alterations in gut microbial composition, can also dysregulate immune responses, causing inflammation, oxidative stress, and insulin resistance. Over time, chronic dysbiosis and the translocation of bacteria and their metabolic products across the mucosal barrier may increase prevalence of type 2 diabetes, cardiovascular disease, inflammatory bowel disease, autoimmune disease, and a variety of cancers. In this paper, we highlight the pivotal role gut microbiota and their metabolites (short-chain fatty acids (SCFAs)) play in mucosal immunity.

摘要

肠道微生物群与宿主的先天和适应性免疫系统之间的动态相互作用在维持肠道稳态和抑制炎症方面发挥着关键作用。肠道微生物群代谢蛋白质和复杂碳水化合物,合成维生素,并产生大量可介导肠道上皮细胞与免疫细胞之间相互作用的代谢产物。作为一种防御机制,肠道上皮细胞产生黏膜屏障,将微生物群与宿主免疫细胞隔离开来,并降低肠道通透性。肠道微生物群与黏膜免疫系统之间的相互作用受损会导致潜在致病性革兰氏阴性菌的丰度增加及其相关的代谢变化,破坏上皮屏障并增加感染易感性。肠道微生物失调,即肠道微生物组成的负面改变,也会使免疫反应失调,导致炎症、氧化应激和胰岛素抵抗。随着时间的推移,慢性微生物失调以及细菌及其代谢产物穿过黏膜屏障的易位可能会增加2型糖尿病、心血管疾病、炎症性肠病、自身免疫性疾病和多种癌症的患病率。在本文中,我们强调了肠道微生物群及其代谢产物(短链脂肪酸(SCFAs))在黏膜免疫中所起的关键作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2893/7602490/fa6db8306766/microorganisms-08-01587-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2893/7602490/8f377b92f833/microorganisms-08-01587-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2893/7602490/36c542e47e46/microorganisms-08-01587-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2893/7602490/fa6db8306766/microorganisms-08-01587-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2893/7602490/8f377b92f833/microorganisms-08-01587-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2893/7602490/36c542e47e46/microorganisms-08-01587-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2893/7602490/fa6db8306766/microorganisms-08-01587-g003.jpg

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