Abstract
Activation of the transcription factor Stat1 by interferon-γ (IFN-γ) is an important step in the development of antimicrobial effector mechanisms against many bacterial pathogens. Susceptibility to murine Lyme arthritis has been correlated with the production of several proinflammatory cytokines, especially IFN-γ. To determine the role of IFN-mediated effector mechanisms in the development of Lyme borreliosis, we infected Stat1-deficient mice on both resistant (DBA), and susceptible (C3H) genetic backgrounds. Arthritis in Stat1–/– mice was similar to that of wild-type controls in both mouse strains. Spirochete loads in tissues were also unchanged in Stat1–/– mice. C3H Stat1–/– mice exhibited increased inflammation in the heart, whereas carditis was unchanged in DBA Stat1–/– mice. These results demonstrate that inhibition of macrophage activation and responses to IFN-γ-mediated signaling do not alter the arthritis resistance or susceptibility phenotype; however, they do affect the severity of carditis in susceptible mouse strains.
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