The Journal of Experimental Medicine
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Published online December 31, 2007
doi:10.1084/jem.20070962
The Journal of Experimental Medicine, Vol. 205, No. 1, 133-141
The Rockefeller University Press, 0022-1007 $30.00
© 2007 Pal et al.
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*Lyme Disease
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ARTICLE

 Borrelia burgdorferi basic membrane proteins A and B participate in the genesis of Lyme arthritis

Utpal Pal1, Penghua Wang1, Fukai Bao1, Xiuli Yang2, Swapna Samanta1, Robert Schoen1, Gary P. Wormser3, Ira Schwartz4, and Erol Fikrig1

1 Section of Rheumatology, Department of Internal Medicine, Yale University School of Medicine, New Haven, CT 06520
2 Department of Veterinary Medicine, University of Maryland, College Park, MD 20742
3 Division of Infectious Diseases, Department of Medicine, and 4 Department of Microbiology and Immunology, New York Medical College, Valhalla, NY 10595

CORRESPONDENCE Erol Fikrig: erol.fikrig{at}yale.edu

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.

Abbreviations used: DECAL, differential expression analysis using a custom-amplified library; GST, glutathione S-transferase; q, quantitative.

U. Pal, P. Wang, and F. Bao contributed equally to this paper.

U. Pal's present address is Department of Veterinary Medicine, University of Maryland, College Park, MD 20742.

F. Bao's present address is Department of Microbiology, Kunming Medical College, Kunming 650031, China.


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