期刊
INFECTION AND IMMUNITY
卷 80, 期 11, 页码 3921-3929出版社
AMER SOC MICROBIOLOGY
DOI: 10.1128/IAI.00806-12
关键词
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资金
- Joint Ph.D. Program under the Strategic Scholarships for Frontier Research Network, Office of the Higher Education Commission, Thailand
- National Institutes of Health, National Institute of Allergy and Infectious Diseases [UO1 AI082110]
- Biotechnology and Biological Sciences Research Council [BBS/E/I/00001116, BBS/E/D/20231761] Funding Source: researchfish
- Grants-in-Aid for Scientific Research [22591116] Funding Source: KAKEN
- BBSRC [BBS/E/D/20231761] Funding Source: UKRI
Burkholderia pseudomallei is the causative pathogen of melioidosis, of which a major predisposing factor is diabetes mellitus. Polymorphonuclear neutrophils (PMNs) kill microbes extracellularly by the release of neutrophil extracellular traps (NETs). PMNs play a key role in the control of melioidosis, but the involvement of NETs in killing of B. pseudomallei remains obscure. Here, we showed that bactericidal NETs were released from human PMNs in response to B. pseudomallei in a dose-and time-dependent manner. B. pseudomallei-induced NET formation required NADPH oxidase activation but not phosphatidylinositol-3 kinase, mitogen-activated protein kinases, or Src family kinase signaling pathways. B. pseudomallei mutants defective in the virulence-associated Bsa type III protein secretion system (T3SS) or capsular polysaccharide I (CPS-I) induced elevated levels of NETs. NET induction by such mutants was associated with increased bacterial killing, phagocytosis, and oxidative burst by PMNs. Taken together the data imply that T3SS and the capsule may play a role in evading the induction of NETs. Importantly, PMNs from diabetic subjects released NETs at a lower level than PMNs from healthy subjects. Modulation of NET formation may therefore be associated with the pathogenesis and control of melioidosis.
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