| Literature DB >> 29044406 |
Seong-Woo Kim1, Bindu Subhadra1, Jake Whang1, Yong Woo Back1, Hyun Shik Bae1, Hwa-Jung Kim1, Chul Hee Choi1.
Abstract
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. © FEMS 2017. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.Entities:
Keywords: Mycobacterium abscessus; autophagy; intracellular survival; lipid; virulence
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Year: 2017 PMID: 29044406 DOI: 10.1093/femspd/ftx107
Source DB: PubMed Journal: Pathog Dis ISSN: 2049-632X Impact factor: 3.166