PE_PGRS62 promotes the survival of Mycobacterium smegmatis within macrophages via disrupting ER stress-mediated apoptosis
PE_PGRS62 promotes the survival of Mycobacterium smegmatis within macrophages via disrupting ER stress-mediated apoptosis
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PE_PGRS62 通过破坏内质网应激介导的细胞凋亡促进巨噬细胞内耻垢分枝杆菌的存活
DOI：
10.1002/jcp.28577
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发表时间：
2019-11-01
影响因子：
5.6
通讯作者：
Deng, Wanyan
中科院分区：
文献类型：
--
作者：
Long, Quanxin;Xiang, Xiaohong;Deng, Wanyan
结核分枝杆菌是结核病的主要病原体，仍然是最致命的传染性病原体之一。 PE_PGRS蛋白因其在分枝杆菌，尤其是致病性分枝杆菌中的物种特异性而成为新的焦点。尽管进行了大量研究，PE_PGRS蛋白仍然是分枝杆菌发病机制的一个神秘方面，其机制尚不清楚。在此，我们重点关注来自结核分枝杆菌的 PE_PGRS 成员 PE_PGRS62，其特征在于破坏吞噬溶酶体成熟的表面暴露蛋白功能。 PE_PGRS62 在耻垢分枝杆菌（一种天然缺乏 PE_PGRS 基因的非病原菌）中表达，可增强巨噬细胞对各种体外应激的抵抗力和细胞存活率。结果，巨噬细胞的细胞因子谱受到干扰，并通过降低内质网应激反应来抑制细胞凋亡。
Mycobacterium tuberculosis, the leading causative agent of tuberculosis, remains one of the most deadly infectious pathogens. PE_PGRS proteins become a new focus as their species specificity in mycobacteria, especially in pathogenic mycobacteria. Despite intensive research, PE_PGRS proteins are still a mysterious aspect of mycobacterial pathogenesis with unknown mechanism. Herein, we focused on a PE_PGRS member from M. tuberculosis, PE_PGRS62, characterized by a surface-exposed protein function in disrupting phagolysosome maturation. Expression of PE_PGRS62 in Mycobacterium smegmatis, a nonpathogenic species naturally deficient in PE_PGRS genes, resulted in enhanced resistance to various in vitro stresses and cellular survival in macrophage. As a consequence, the cytokine profiles of macrophage were disturbed and cell apoptosis were inhibited via decreasing endoplasmic reticulum stress response.