期刊
JOURNAL OF EXPERIMENTAL MEDICINE
卷 205, 期 1, 页码 133-141出版社
ROCKEFELLER UNIV PRESS
DOI: 10.1084/jem.20070962
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Lyme arthritis results from colonization of joints by Borrelia burgdorferi and the ensuing host response. Using gene array-based differential analysis of B. burgdorferi gene expression and quantitative reverse trancription- polymerase chain reaction, we identified two paralogous spirochete genes, bmpA and bmpB, that are preferentially up-regulated in mouse joints compared with other organs. Transfer of affinity-purified antibodies against either BmpA or BmpB into B. burgdorferi-infected mice selectively reduced spirochete numbers and inflammation in the joints. B. burgdorferi lacking bmpA/B were therefore generated to further explore the role of these proteins in the pathogenesis of Lyme disease. B. burgdorferi lacking bmpA/B were infectious in mice, but unable to persist in the joints, and they failed to induce severe arthritis. Complementation of the mutant spirochetes with a wild-type copy of the bmpA and bmpB genes partially restored the original phenotype. These data delineate a role for differentially produced B. burgdorferi antigens in spirochete colonization of mouse joints, and suggest new strategies for the treatment of Lyme arthritis.
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