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Infection and Immunity, March 2008, p. 1239-1246, Vol. 76, No. 3
0019-9567/08/$08.00+0     doi:10.1128/IAI.00897-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

Both Decorin-Binding Proteins A and B Are Critical for the Overall Virulence of Borrelia burgdorferi

Department of Pathobiological Sciences, Louisiana State University, Baton Rouge, Louisiana 70803

Received 2 July 2007/ Returned for modification 27 September 2007/ Accepted 31 December 2007

Both decorin-binding proteins (DbpA and DbpB) of the Lyme disease spirochete Borrelia burgdorferi bind decorin and glycosaminoglycans, two important building blocks of proteoglycans that are abundantly found in the extracellular matrix (ECM) and connective tissues as well as on cell surfaces of mammals. As an extracellular pathogen, B. burgdorferi resides primarily in the ECM and connective tissues and between host cells during mammalian infection. The interactions of B. burgdorferi with these host ligands mediated by DbpA and DbpB potentially influence various aspects of infection. Here, we show that both DbpA and DbpB are critical for the overall virulence of B. burgdorferi in the murine host. Disruption of the dbpBA locus led to nearly a 10⁴-fold increase in the 50% infectious dose (ID₅₀). Complementation of the mutant with either dbpA or dbpB reduced the ID₅₀ from over 10⁴ to roughly 10³ organisms. Deletion of the dbpBA locus affected colonization in all tissues of infected mice. The lack of dbpA alone precluded the pathogen from colonizing the heart tissue, and B. burgdorferi deficient for DbpB was recovered only from 42% of the heart specimens of infected mice. Although B. burgdorferi lacking either dbpA or dbpB was consistently grown from joint specimens of almost all infected mice, it generated bacterial loads significantly lower than the control. The deficiency in either DbpA or DbpB did not reduce the bacterial load in skin, but lack of both significantly did. Taken together, the study results indicate that neither DbpA nor DbpB is essential for mammalian infection but that both are critical for the overall virulence of B. burgdorferi.

Published ahead of print on 14 January 2008.

Editor: V. J. DiRita

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