Abstract
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.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, U.S. Gov't, Non-P.H.S.
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Review
MeSH terms
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Enzyme Activation
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Francisella tularensis / immunology
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Francisella tularensis / pathogenicity
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Francisella tularensis / physiology*
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Helicobacter pylori / immunology
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Helicobacter pylori / pathogenicity
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Helicobacter pylori / physiology*
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Humans
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Immunity, Innate
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Microbial Viability
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NADPH Oxidases / immunology
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NADPH Oxidases / metabolism*
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Neutrophil Activation
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Neutrophils / immunology
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Neutrophils / metabolism*
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Neutrophils / microbiology*
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Phagocytosis
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Phagosomes / immunology
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Phagosomes / metabolism*