Abstract
In mice, Anaplasma phagocytophilum control is independent of phagocyte oxidase (phox), inducible NO synthase (NOS2), tumor necrosis factor (TNF), and MyD88 Toll-like receptor signaling. We show that despite evasion of these host responses, phox, NOS2, TNF, and MyD88 are activated and contribute to inflammation and hepatic injury more than A. phagocytophilum itself.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
MeSH terms
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Adaptor Proteins, Signal Transducing / genetics
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Adaptor Proteins, Signal Transducing / metabolism
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Anaplasma phagocytophilum / immunology*
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Animals
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Disease Models, Animal
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Ehrlichiosis / immunology*
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Ehrlichiosis / microbiology
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Ehrlichiosis / physiopathology*
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Humans
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Immunity, Innate*
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Inflammation
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Liver Diseases / immunology*
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Liver Diseases / microbiology
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Liver Diseases / physiopathology*
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Mice
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Mice, Inbred C3H
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Mice, Knockout
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Mice, SCID
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Myeloid Differentiation Factor 88
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Nitric Oxide Synthase Type II / genetics
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Nitric Oxide Synthase Type II / metabolism
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Oxidoreductases / genetics
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Oxidoreductases / metabolism
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Phagocytes / enzymology
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Tumor Necrosis Factors / genetics
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Tumor Necrosis Factors / metabolism
Substances
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Adaptor Proteins, Signal Transducing
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MYD88 protein, human
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Myd88 protein, mouse
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Myeloid Differentiation Factor 88
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Tumor Necrosis Factors
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Oxidoreductases
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Nitric Oxide Synthase Type II
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Nos2 protein, mouse