内质网应激在寄生虫感染中的作用  

Effects of endoplasmic reticulum stress in parasite infection

作　　者：魏绮珮 齐永芬[1,2] 鱼艳荣[1] WEI Qi-pei;QI Yong-fen;YU Yan-rong(Department of Pathogen Biology;Laboratory of Bioactive Molecule, School of Basic Medical Sciences, Peking University, Beijing 100191, China)

机构地区：[1]北京大学基础医学院病原生物学系,北京100191 [2]北京大学基础医学院生物活性小分子研究室,北京100191

出　　处：《中国寄生虫学与寄生虫病杂志》2017年第6期617-622,共6页Chinese Journal of Parasitology and Parasitic Diseases

基　　金：国家自然科学基金(No.30901247);国家基础科学人才培养基金(No.J1030831/J0108)

摘　　要：在感染及其他各种应激条件下,内质网由于蛋白分泌过多或错误折叠蛋白过多导致内质网稳态失衡称为内质网应激。内质网应激会引起一系列的信号和转录事件,称为未折叠蛋白反应。未折叠蛋白反应可通过减少翻译,帮助蛋白折叠以及降解错误折叠蛋白来恢复内质网的稳态,但长期的、严重的内质网应激则引起应激细胞的凋亡和局部炎症。在寄生虫感染中,由于虫体寄生诱发了宿主细胞的内质网应激并启动未折叠蛋白反应,而寄生虫可通过各种方式利用这一反应来促进自身的存活和对宿主的致病作用,并影响宿主细胞的炎症、氧化应激、凋亡及免疫反应。本文综述了近年来内质网应激在寄生虫感染致病中的作用的研究进展,为寄生虫与宿主的相互关系研究及寄生虫病的防治提供新的线索和思路。Endoplasmic reticulum stress （ERS） is a disorder of endoplasmic reticulum homeostasis caused by excessive secretion of proteins or protein misfolding under infection and other stressors. ERS triggers a series of signaling and transcriptional events, termed unfolded protein response （UPR）. Although UPR can restore endoplasmic reticulum homeostasis by reducing protein translation, aiding protein folding and degrading misfolded protein, long- term, serious ERS causes apoptosis of stressed cells and local inflammation. During infection of parasites, ERS is induced in host cells, together with initiation of UPR. The parasites can use this reaction in various ways to promote its survival and pathogenicity, and to influence inflammation, oxidative stress, apoptosis and immune responses of host cells. This review summarizes research progress on the effects of ERS in parasite infection, in the aim to provide new clues and ideas for investigating the relationship between parasites and host, and the control of parasitic diseases.

关 键 词：寄生虫感染 内质网应激 原虫 蠕虫 

分 类 号：R53[医药卫生—内科学]