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Title: Neutrophil extracellular traps exhibit antibacterial activity against Burkholderia pseudomallei and are influenced by bacterial and host factors
Authors: Donporn Riyapa
Surachat Buddhisa
Sunee Korbsrisate
Jon Cuccui
Brendan W. Wren
Mark P. Stevens
Manabu Ato
Ganjana Lertmemongkolchai
Khon Kaen University
Mahidol University
London School of Hygiene & Tropical Medicine
University of Edinburgh, Roslin Institute
National Institute of Infectious Diseases
Keywords: Immunology and Microbiology;Medicine
Issue Date: 1-Nov-2012
Citation: Infection and Immunity. Vol.80, No.11 (2012), 3921-3929
Abstract: 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 phosphatidylinosi-tol-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. © 2012, American Society for Microbiology.
ISSN: 10985522
Appears in Collections:Scopus 2011-2015

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