期刊
AUTOPHAGY
卷 11, 期 5, 页码 748-755出版社
TAYLOR & FRANCIS INC
DOI: 10.1080/15548627.2015.1040969
关键词
autophagy; Burkholderia pseudomallei; LC3-II; melioidosis; neutrophils; T3SS
类别
资金
- National Institutes of Health: NIAID Cooperative Center for Translational Research on Human Immunology and Biodefense [U01 AI0 82110]
- Faculty of Associated Medical Sciences, Khon Kaen University (AMS Incubator Postdoctoral Training Program)
- Thailand Research Fund through the Royal Golden Jubilee Ph.D. Program [PHD/0215/2550]
- Ministry of Education, Science, Sports and Culture of Japan [18076005]
- Ministry of Health, Labor and Welfare of Japan
- Grants-in-Aid for Scientific Research [26111519, 25460276, 15H01388] Funding Source: KAKEN
- Biotechnology and Biological Sciences Research Council [BBS/E/I/00001116, BBS/E/D/20231761] Funding Source: researchfish
- BBSRC [BBS/E/D/20231761] Funding Source: UKRI
Neutrophils play a key role in the control of Burkholderia pseudomallei, the pathogen that causes melioidosis. Here, we show that survival of intracellular B. pseudomallei was significantly increased in the presence of 3-methyladenine or lysosomal cathepsin inhibitors. The LC3-flux was increased in B. pseudomallei-infected neutrophils. Concordant with this result, confocal microscopy analyses using anti-LC3 antibodies revealed that B. pseudomallei-containing phagosomes partially overlapped with LC3-positive signal at 3 and 6h postinfection. Electron microscopic analyses of B. pseudomallei-infected neutrophils at 3h revealed B. pseudomallei-containing phagosomes that occasionally fused with phagophores or autophagosomes. Following infection with a B. pseudomallei mutant lacking the Burkholderia secretion apparatus Bsa Type III secretion system, neither this characteristic structure nor bacterial escape into the cytosol were observed. These findings indicate that human neutrophils are able to recruit autophagic machinery adjacent to B. pseudomallei-containing phagosomes in a Type III secretion system-dependent manner.
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