Abstract
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.