Clinical Mycobacterium abscessus strain inhibits autophagy flux and promotes its growth in murine macrophages

被引：23

作者：

Kim, Seong-Woo ^{[1
]}

Subhadra, Bindu ^{[1
]}

Whang, Jake ^{[1
]}

Back, Yong Woo ^{[1
]}

Bae, Hyun Shik ^{[1
]}

Kim, Hwa-Jung ^{[1
]}

Choi, Chul Hee ^{[1
]}

机构：

[1] Chungnam Natl Univ, Sch Med, Dept Microbiol & Med Sci, 266 Munwha Ro, Daejeon 35015, South Korea

来源：

PATHOGENS AND DISEASE | 2017年 / 75卷 / 08期

基金：

新加坡国家研究基金会;

关键词：

Mycobacterium abscessus; autophagy; virulence; intracellular survival; lipid; MYO-INOSITOL MANNOSIDES; TUBERCULOSIS; BACTERIA; PATHWAY; SURFACE; INNATE; LIPIDS; P62; GLYCOPEPTIDOLIPIDS; LIPOARABINOMANNAN;

D O I：

10.1093/femspd/ftx107

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

Autophagy is known to be a vital homeostatic defense process that controls mycobacterial infection. However, the relationship between autophagy response and the virulence of Mycobacterium abscessus strain UC22 has not been reported. Here, we demonstrate that M. abscessus induces autophagy and inhibits autophagy flux in murine macrophages. Further, the rough variant of M. abscessus, UC22 that is a highly virulent clinical isolate, significantly inhibited autophagic flux than the smooth variant of M. abscessus ATCC 19977. In addition, it was noticed that the intracellular survival of UC22 is significantly enhanced by blocking the autophagosome-lysosome fusion in macrophages compared to the smooth variant. However, Mycobacterium smegmatis did not block autophagy flux in murine macrophages. Besides, we confirmed that the lipid components of M. abscessus UC22 play a role in autophagosome formation. These data suggest that the virulent M. abscessus might be able to survive and grow within autophagosomes by preventing the autophagosome-lysosome fusion and their clearance from the cells.

引用

页数：8

共 48 条

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