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Anaplasma phagocytophilum , interferon gamma production and Stat1 signaling
Author(s) -
Choi KyoungSeong,
Dumler J. Stephen
Publication year - 2013
Publication title -
microbiology and immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.664
H-Index - 70
eISSN - 1348-0421
pISSN - 0385-5600
DOI - 10.1111/1348-0421.12023
Subject(s) - anaplasma phagocytophilum , biology , stat1 , stat protein , immunology , intracellular parasite , obligate , proinflammatory cytokine , interferon gamma , interferon , virology , cytokine , microbiology and biotechnology , inflammation , signal transduction , immune system , stat3 , antibody , ecology , borrelia burgdorferi
Human granulocytic anaplasmosis is caused by the obligate intracellular bacterium, Anaplasma phagocytophilum . The proinflammatory cytokine, IFN‐γ, is necessary for innate immunity and plays an important role in the induction of severe histopathology in A. phagocytophilum ‐infected mice, horses and humans. In this study, activation of signal transducer and activator of transcription (Stat) 1 phosphorylation associated with A. phagocytophilum infection was examined in mice and found to be markedly greater on day 7 post‐infection than in mock‐infected controls. This increase in phosphorylated Stat1 (pStat1) correlated significantly with IFN‐γ production and inflammatory tissue injury. Because pStat1 operates as a transcription factor central to the generation of effectors of inflammatory injury, these data suggest that Stat1 signaling is involved in IFN‐γ‐mediated immunopathologic lesions and disease in A. phagocytophilum infection and could be an important target for intervention in this disease.