Shuttling of information between the mucosal and luminal environment drives intestinal homeostasis

被引:43
作者
Asselin, Claude [1 ]
Gendron, Fernand-Pierre [1 ]
机构
[1] Univ Sherbrooke, Fac Med & Sci Sante, Dept Anat & Biol Cellulaire, Sherbrooke, PQ J1E 4K8, Canada
关键词
Goblet and Paneth cell; T-regulatory cell; Ah receptor; ER stress and autophagy; Butyrate; HDAC; ARYL-HYDROCARBON RECEPTOR; INNATE LYMPHOID-CELLS; REGULATORY T-CELLS; CHAIN FATTY-ACIDS; SEGMENTED FILAMENTOUS BACTERIA; ENDOPLASMIC-RETICULUM STRESS; PANETH CELLS; EPITHELIAL-CELLS; GUT MICROBIOTA; ER STRESS;
D O I
10.1016/j.febslet.2014.02.049
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
070307 [化学生物学]; 071010 [生物化学与分子生物学];
摘要
The gastrointestinal tract is a passageway for dietary nutrients, microorganisms and xenobiotics. The gut is home to diverse bacterial communities forming the microbiota. While bacteria and their metabolites maintain gut homeostasis, the host uses innate and adaptive immune mechanisms to cope with the microbiota and luminal environment. In recent years, multiple bi-directional instructive mechanisms between microbiota, luminal content and mucosal immune systems have been uncovered. Indeed, epithelial and immune cell-derived mucosal signals shape microbiota composition, while microbiota and their by-products shape the mucosal immune system. Genetic and environmental perturbations alter gut mucosal responses which impact on microbial ecology structures. On the other hand, changes in microbiota alter intestinal mucosal responses. In this review, we discuss how intestinal epithelial Paneth and goblet cells interact with the microbiota, how environmental and genetic disorders are sensed by endoplasmic reticulum stress and autophagy responses, how specific bacteria, bacterial- and diet-derived products determine the function and activation of the mucosal immune system. We will also discuss the critical role of HDAC activity as a regulator of immune and epithelial cell homeostatic responses. (C) 2014 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.
引用
收藏
页码:4148 / 4157
页数:10
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