To activate or not to activate: distinct strategies used by Helicobacter pylori and Francisella tularensis to modulate the NADPH oxidase and survive in human neutrophils.
Neutrophils accumulate rapidly at sites of infection, and the ability of these cells to phagocytose and kill microorganisms is an essential component of the innate immune response. Relatively few microbial pathogens are able to evade neutrophil killing. Herein, we describe the novel strategies used by Helicobacter pylori and Francisella tularensis to disrupt neutrophil function, with a focus on assembly and activation of the nicotinamide adenine dinucleotide phosphate (NADPH) oxidase.
Allen
Lee-Ann H
LA
Inflammation Program, Department of Internal Medicine, University of Iowa, VA Medical Center, Iowa City, IA 52241, USA. lee-ann-allen@uiowa.edu
McCaffrey
Ramona L
RL
D004789:Enzyme Activation; D005604:Francisella tularensis / Q000276:immunology / Q000472:pathogenicity / Q000502:physiology*; D016480:Helicobacter pylori / Q000276:immunology / Q000472:pathogenicity / Q000502:physiology*; D006801:Humans; D007113:Immunity, Innate; D050296:Microbial Viability; D019255:NADPH Oxidases / Q000276:immunology / Q000378:metabolism*; D018375:Neutrophil Activation; D009504:Neutrophils / Q000276:immunology / Q000378:metabolism* / Q000382:microbiology*; D010587:Phagocytosis; D010588:Phagosomes / Q000276:immunology / Q000378:metabolism*
D019255:NADPH Oxidases