Abstract
The pulmonary innate response to low-dose bacterial challenge requires functioning alveolar macrophages (AM) but also subsequent macrophage apoptosis. To address the role of reactive oxygen species (ROS) and nitric oxide (NO) in AM apoptosis, sub-clinical Streptococcus pneumoniae infection was established in gp91(phox-/-) and inducible NO synthase deficient (iNOS(-/-)) mice. Both AM apoptosis and the number of macrophages containing apoptotic bodies are reduced in iNOS(-/-) as compared to control or gp91(phox-/-) mice. iNOS(-/-) mice recruit neutrophils and generate TNF-alpha to compensate for impaired AM competence but ROS deficiency has no apparent effect on AM function in this model.
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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Female
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Immunity, Innate / immunology
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Lung / microbiology*
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Macrophages, Alveolar / immunology*
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Macrophages, Alveolar / metabolism
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Membrane Glycoproteins / deficiency
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Mice
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Mice, Inbred C57BL
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NADPH Oxidase 2
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NADPH Oxidases / deficiency
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Nitric Oxide / immunology*
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Nitric Oxide / metabolism
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Nitric Oxide Synthase Type II / deficiency
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Pneumococcal Infections / immunology*
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Pneumococcal Infections / metabolism
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Reactive Oxygen Species / immunology*
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Reactive Oxygen Species / metabolism
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Streptococcus pneumoniae / immunology*
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Streptococcus pneumoniae / metabolism
Substances
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Membrane Glycoproteins
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Reactive Oxygen Species
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Nitric Oxide
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Nitric Oxide Synthase Type II
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Nos2 protein, mouse
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Cybb protein, mouse
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NADPH Oxidase 2
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NADPH Oxidases