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Infection and Immunity, June 2006, p. 3305-3313, Vol. 74, No. 6
0019-9567/06/$08.00+0     doi:10.1128/IAI.02035-05
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

Borrelia burgdorferi Lacking BBK32, a Fibronectin-Binding Protein, Retains Full Pathogenicity

Xin Li,1 Xianzhong Liu,1 Deborah S. Beck,1 Fred S. Kantor,2 and Erol Fikrig1*

Sections of Rheumatology,1 Allergy and Immunology, Department of Internal Medicine, Yale University School of Medicine, New Haven, Connecticut 06520-80312

Received 19 December 2005/ Returned for modification 31 January 2006/ Accepted 10 March 2006

BBK32, a fibronectin-binding protein of Borrelia burgdorferi, is one of many surface lipoproteins that are differentially expressed by the Lyme disease spirochete at various stages of its life cycle. The level of BBK32 expression in B. burgdorferi is highest during infection of the mammalian host and lowest in flat ticks. This temporal expression profile, along with its fibronectin-binding activity, strongly suggests that BBK32 may play an important role in Lyme pathogenesis in the host. To test this hypothesis, we constructed an isogenic BBK32 deletion mutant from wild-type B. burgdorferi B31 by replacing the BBK32 gene with a kanamycin resistance cassette through homologous recombination. We examined both the wild-type strain and the BBK32 deletion mutant extensively in the experimental mouse-tick model of the Borrelia life cycle. Our data indicated that B. burgdorferi lacking BBK32 retained full pathogenicity in mice, regardless of whether mice were infected artificially by syringe inoculation or naturally by tick bite. The loss of BBK32 expression in the mutant had no adverse effect on spirochete acquisition (mouse-to-tick) and transmission (tick-to-mouse) processes. These results suggest that additional B. burgdorferi proteins can complement the function of BBK32, fibronectin binding or otherwise, during the natural spirochete life cycle.

* Corresponding author. Mailing address: Section of Rheumatology, Department of Internal Medicine, Yale University School of Medicine, 300 Cedar St., New Haven, CT 06520-8031. Phone: (203) 785-2453. Fax: (203) 785-7053. E-mail: erol.fikrig{at}yale.edu.

Editor: D. L. Burns

Infection and Immunity, June 2006, p. 3305-3313, Vol. 74, No. 6
0019-9567/06/$08.00+0     doi:10.1128/IAI.02035-05
Copyright © 2006, American Society for Microbiology. All Rights Reserved.



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