Key result
In murine Lyme carditis, early up-regulation of proinflammatory cytokines (IL-1beta, TNF-alpha) is followed by sustained expression of the Th1 cytokine IFN-gamma, with no detectable IL-4.
This study identifies the temporal cytokine expression pattern in murine Lyme carditis, demonstrating an early proinflammatory response followed by a sustained Th1 response.
Suggests Th1-dominant immune response in Lyme carditis; leaves open whether cytokine targeting alters outcomes in humans.
The cardiac infiltrate seen in murine Lyme carditis is composed predominantly of macrophages, but small numbers of T cells are also present. To identify the cytokines present in cardiac lesions from susceptible mice, semiquantitative polymerase chain reaction was done on cardiac tissue from mice infected with Borrelia burgdorferi. The temporal expression of proinflammatory and T cell-derived cytokines was characterized in cardiac tissue at days 0, 3, 7, 14, 21, and 42 after infection with B. burgdorferi. Early in the course of infection, up-regulation of the proinflammatory cytokines interleukin-1beta and tumor necrosis factor-alpha was detected. The Th1 cytokine interferon-gamma appeared after the expression of the proinflammatory cytokines and remained elevated throughout the study. Interleukin-4 was not detectable at any time in cardiac lesions. These data are the first to identify cytokines expressed at the lesional level in murine Lyme carditis and to demonstrate a Th1 pattern of cytokine expression in this lesion.
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Doyle et al. (1998) studied Murine Lyme carditis. Borrelia burgdorferi infection was evaluated on Temporal expression of proinflammatory and T cell-derived cytokines in cardiac tissue. In murine Lyme carditis, early up-regulation of proinflammatory cytokines (IL-1beta, TNF-alpha) is followed by sustained expression of the Th1 cytokine IFN-gamma, with no detectable IL-4.
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