结核分枝杆菌分泌蛋白调控巨噬细胞自噬诱导持续性感染  

Mycobacterium Tuberculosis Secretory Protein Regulates Macrophages Autophagy-induced Persistent Infection

作　　者：张彩勤[1] 杨丽[1] 张廷芬 师长宏[1] ZHANG Cai-qin;YANG Li;ZHANG Ting-fen;SHI Chang-hong(Lab Animal Center,The Fourth Military Medical University,Xi an 710032,China;Chinese People s Liberation Army Institute for Disease Control and Prevention,Beijing 100071,China)

机构地区：[1]第四军医大学实验动物中心,西安710032 [2]解放军疾病预防控制所,北京100071

出　　处：《科学技术与工程》2018年第32期124-128,共5页Science Technology and Engineering

基　　金：国家自然科学基金(31501112)资助

摘　　要：巨噬细胞的自噬作用能够保护宿主抵抗结核分枝杆菌的感染;而持续性感染的MTB(Mycobacterium tuberculosis)可以从自噬体中逃逸或抑制自噬的发生,从而在宿主体内长期存活。尽管相关机制不明确,但胞内存活的MTB分泌蛋白在持续性感染时发挥了重要作用。它可以通过抑制巨噬细胞自噬维持蛋白质稳定性和在胞内长期存活,导致LTBI(latent TB infection)的发生。综述了MTB的四种分泌蛋白(Eis、Pkn G、Sap M和Hsp16. 3)在持续性感染中调节巨噬细胞自噬的作用,可能为发现LTBI新的生物标志物和药物新靶点提供有效思路。Macrophage autophagy plays an important role in protecting the host against tuberculosis.The persistently infected Mycobacterium tuberculosis(MTB)can escape from the autophagosome or inhibit autophagy,and survive within the host for an extended period of time.Although the underlying mechanism is unclear,the secreted proteins of intracellular surviving MTB have been reported to contribute to TB persistence.They can maintain the stability of proteins and survive in the macrophage for a long time by inhibiting autophagy,which leaded to the occurrence of latent Mycobacterium tuberculosis infection(LTBI).This review focused on the role of the four secretory proteins(Eis,PknG,SapM and Hsp16.3)of MTB about regulating macrophage autophagy in MTB persistent infection.It may provide an effective idea for the discovery of potential biomarkers of LTBI and targets of novel drugs.

关 键 词：结核分枝杆菌 分泌蛋白 巨噬细胞自噬 持续性感染 

分 类 号：R378.91[医药卫生—病原生物学]