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Infection and Immunity, March 2000, p. 1222-1230, Vol. 68, No. 3
0019-9567/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.

Borrelia burgdorferi Gene Expression In Vivo and Spirochete Pathogenicity

Juan Anguita,1 Swapna Samanta,1 Beatriz Revilla,1 Kyoungho Suk,1,dagger Subrata Das,1 Stephen W. Barthold,2 and Erol Fikrig1,*

Section of Rheumatology, Department of Internal Medicine, Yale University School of Medicine, New Haven, Connecticut 06520,1 and Center for Comparative Medicine, Schools of Medicine and Veterinary Medicine, University of California at Davis, Davis, California 956162

Received 13 October 1999/Returned for modification 19 November 1999/Accepted 30 November 1999

Borrelia burgdorferi spirochetes that do not cause arthritis or carditis were developed and used to investigate Lyme disease pathogenesis. A clonal isolate of B. burgdorferi N40 (cN40), which induces disease in C3H/HeN (C3H) mice, was repeatedly passaged in vitro to generate nonpathogenic spirochetes. The passage 75 isolate (N40-75) was infectious for C3H mice but did not cause arthritis or carditis, and spirochetes were at low levels or absent in the joints or hearts, respectively. N40-75 could, however, cause disease in severe combined immunodeficient (SCID) mice, suggesting that the response in immunocompetent mice prevented effective spirochete dissemination and the subsequent development of arthritis and carditis. Administration of immune sera at 4 days after spirochete challenge aborted N40-75, but not cN40, infection in SCID mice. A B. burgdorferi genomic expression library was differentially probed with sera from cN40- and N40-75-infected mice, to identify genes that may not be effectively expressed by N40-75 in vivo. N40-75 was defective in the up-regulation of several genes that are preferentially expressed during mammalian infection, including dbpAB, bba64, and genes that map to the cp32 family of plasmids. These data suggest that adaptation and gene expression may be required for B. burgdorferi to effectively colonize the host, evade humoral responses, and cause disease.

* Corresponding author. Mailing address: 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: ef6{at}emailmed.yale.edu.

dagger Present address: Samsung Biomedical Research Institute, Clinical Research Center, Seoul, South Korea 135-230.

Infection and Immunity, March 2000, p. 1222-1230, Vol. 68, No. 3
0019-9567/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.


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