Abstract
Clearance of senescent cells from damaged tissue is a crucial step to successfully resolve an inflammatory response. Poor clearance has been attributed to defects in neutrophil apoptosis, a process that is regulated in part by reactive oxygen species (ROS) produced by activated neutrophils. Using ROS-deficient and wild-type macrophages treated with extracellular ROS scavengers we demonstrate that macrophage-derived ROS also influence phagocytosis and do so by direct and indirect mechanisms.
(c) 2009 S. Karger AG, Basel.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Apoptosis / immunology
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Cell Separation
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Flow Cytometry
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Humans
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Macrophages / immunology*
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Macrophages / metabolism
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Membrane Glycoproteins / deficiency
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Membrane Glycoproteins / genetics
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Mice
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Mice, Inbred C57BL
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Mice, Knockout
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NADPH Oxidase 2
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NADPH Oxidases / deficiency
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NADPH Oxidases / genetics
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NADPH Oxidases / immunology
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NADPH Oxidases / metabolism
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Neutrophils / immunology
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Neutrophils / pathology
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Phagocytosis / physiology*
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Reactive Oxygen Species / immunology*
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Reactive Oxygen Species / metabolism
Substances
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Membrane Glycoproteins
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Reactive Oxygen Species
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Cybb protein, mouse
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NADPH Oxidase 2
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NADPH Oxidases