Published 15 July 2002. doi:10.1084/jem.20020770
© Rockefeller University Press, 0022-1007/2002/7/275/ $5.00
The Journal of Experimental Medicine, Volume 196, Number 2, July 15, 2002 275-280
Molecular Adaptation of Borrelia burgdorferi in the Murine Host
Fang Ting Liang1,
F. Kenneth Nelson2 and
Erol Fikrig1
1 Section of Rheumatology, Department of Internal Medicine, School of Medicine
2 Department of Molecular, Cellular and Developmental Biology, Yale University, New Haven, CT 06520
Address correspondence to Erol Fikrig, 608 Laboratory of Clinical Investigation, Section of Rheumatology, Department of Internal Medicine, Yale University School of Medicine, 333 Cedar St., New Haven, CT 06520-8031. Phone: 203-785-2453; Fax: 203-785-7053; E-mail: erol.fikrig{at}yale.edu
An analysis of expression of 137 lipoprotein genes on the course of murine infection revealed a two-step molecular adaptation by Borrelia burgdorferi, the Lyme disease spirochete. For the first step, regardless whether the initial inocula of B. burgdorferi expressed either all (cultured spirochetes) or less than 40 (host-adapted spirochetes) of the 137 lipoprotein genes, the spirochetes were modulated to transcribe 116 of the genes within 10 d after being introduced to the murine host. This step of adaptation was induced by the microenvironment of the host tissue. During the second step, which was forced by host immune selection pressure and occurred between 17 and 30 d after infection, B. burgdorferi down-regulated most of the lipoprotein genes and expressed less than 40 of the 137 genes. This novel adaptation mechanism could be a critical step for B. burgdorferi to proceed to chronic infection, as the pathogen would be cleared at the early stage of infection if the spirochetes failed to undergo this process.
Key Words: Lyme disease • immune evasion • lipoprotein • gene expression • DNA microarray
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