Department of Gastroenterology, Changhai Hospital, Second Military Medical University and Naval Medical University, Shanghai, China.
Department of Pharmocology, Second Military Medical University and Naval Medical University, Shanghai, China.
Front Immunol. 2018 Apr 5;9:693. doi: 10.3389/fimmu.2018.00693. eCollection 2018.
Intestinal mucosal barrier, mainly consisting of the mucus layer and epithelium, functions in absorbing nutrition as well as prevention of the invasion of pathogenic microorganisms. Paneth cell, an important component of mucosal barrier, plays a vital role in maintaining the intestinal homeostasis by producing antimicrobial materials and controlling the host-commensal balance. Current evidence shows that the dysfunction of intestinal mucosal barrier, especially Paneth cell, participates in the onset and progression of inflammatory bowel disease (IBD). Autophagy, a cellular stress response, involves various physiological processes, such as secretion of proteins, production of antimicrobial peptides, and degradation of aberrant organelles or proteins. In the recent years, the roles of autophagy in the pathogenesis of IBD have been increasingly studied. Here in this review, we mainly focus on describing the roles of Paneth cell autophagy in IBD as well as several popular autophagy-related genetic variants in Penath cell and the related therapeutic strategies against IBD.
肠黏膜屏障主要由黏液层和上皮细胞组成,具有吸收营养和防止病原微生物侵袭的功能。潘氏细胞作为黏膜屏障的重要组成部分,通过产生抗菌物质和控制宿主共生平衡,在维持肠道内环境稳定方面发挥着重要作用。目前的证据表明,肠黏膜屏障功能障碍,尤其是潘氏细胞功能障碍,参与了炎症性肠病(IBD)的发病和进展。自噬是一种细胞应激反应,涉及多种生理过程,如蛋白质分泌、抗菌肽产生以及异常细胞器或蛋白质的降解。近年来,自噬在 IBD 发病机制中的作用得到了越来越多的研究。在本文中,我们主要集中描述潘氏细胞自噬在 IBD 中的作用,以及潘氏细胞中几种流行的与自噬相关的遗传变异,以及针对 IBD 的相关治疗策略。