ASSOCIATION OF MACROPHAGE INFLAMMATORY RESPONSE AND CELL DEATH AFTER IN VITRO BORRELIA BURGDORFERI INFECTION WITH ARTHRITIS RESISTANCE

LISA J. GLICKSTEIN Center for Immunology and Inflammatory Diseases, Massachusetts General Hospital, Boston, Massachusetts; Division of Geographic Medicine and Infectious Diseases, Tufts-New England Medical Center, Boston, Massachusetts

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JENIFER L. COBURN Center for Immunology and Inflammatory Diseases, Massachusetts General Hospital, Boston, Massachusetts; Division of Geographic Medicine and Infectious Diseases, Tufts-New England Medical Center, Boston, Massachusetts

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Susceptibility to Borrelia burgdorferi infection and subsequent arthritis is genetically determined in mice and determined by innate immunity. Accordingly, macrophage responses to B. burgdorferi challenge may differ between mouse strains. Bone marrow–derived macrophages were infected ex vivo with clonal B. burgdorferi strain N40. Interleukin-12 and tumor necrosis factor-α (TNF-α) production were higher in macrophages from resistant C57Bl/6 mice than in macrophages from susceptible C3H/HeJ mice. However, TNF-α production was observed in lower concentrations in C3H/HeJ (toll-like receptor-4−/−) macrophages than in C3H/FeJ (TLR4+/+) macrophages, suggesting that TLR4 might contribute to the response to B. burgdorferi. A higher cytokine response to B. burgdorferi was associated with cell death in macrophages from resistant C57Bl/6 mice. Understanding variability in the response of macrophages to B. burgdorferi may contribute to understanding Lyme arthritis.

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