Abstract
Mice deficient in phox (gp91(phox-/-)) or NOS2 (NOS2(-/-)) were infected with the agent of human granulocytic ehrlichiosis (HGE) to evaluate the importance of these pathways in the eradication of HGE bacteria. NOS2(-/-) mice had delayed clearance of the HGE agent in comparison to control or gp91(phox-/-) mice, suggesting that reactive nitrogen intermediates play a role in the early control of HGE.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Animals
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Base Sequence
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DNA Primers / genetics
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Ehrlichia / genetics
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Ehrlichia / isolation & purification
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Ehrlichia / pathogenicity
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Ehrlichiosis / enzymology
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Ehrlichiosis / etiology*
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Ehrlichiosis / immunology
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Granulocytes / enzymology
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Granulocytes / immunology
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Humans
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Membrane Glycoproteins / deficiency*
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Membrane Glycoproteins / genetics
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Mice
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Mice, Knockout
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NADPH Oxidase 2
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NADPH Oxidases*
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Nitric Oxide Synthase / deficiency*
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Nitric Oxide Synthase / genetics
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Nitric Oxide Synthase Type II
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Nitrogen / metabolism
Substances
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DNA Primers
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Membrane Glycoproteins
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NOS2 protein, human
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Nitric Oxide Synthase
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Nitric Oxide Synthase Type II
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Nos2 protein, mouse
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CYBB protein, human
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NADPH Oxidase 2
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NADPH Oxidases
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Nitrogen