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Infection and Immunity, December 2008, p. 5694-5705, Vol. 76, No. 12
0019-9567/08/$08.00+0     doi:10.1128/IAI.00690-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

Borrelia burgdorferi Lacking DbpBA Exhibits an Early Survival Defect during Experimental Infection{triangledown}

Eric H. Weening,1 Nikhat Parveen,2 Jerome P. Trzeciakowski,3 John M. Leong,4 Magnus Höök,5 and Jonathan T. Skare1*

Department of Microbial and Molecular Pathogenesis,1 Systems Biology and Translational Medicine, College of Medicine, Texas A&M Health Science Center, College Station, Texas 77843-1114,3 Department of Microbiology and Molecular Genetics, University of Medicine and Dentistry of New Jersey, Newark, New Jersey 07103,2 Department of Molecular Genetics and Microbiology, University of Massachusetts Medical School, Worcester, Massachusetts 01655,4 Center for Extracellular Matrix Biology, Institute of Biosciences and Technology, Texas A&M Health Science Center, Houston, Texas 770305

Received 2 June 2008/ Returned for modification 11 July 2008/ Accepted 10 September 2008

Several Borrelia burgdorferi genes induced under mammalian host conditions have been purported to be important in Lyme disease pathogenesis based on their binding to host structures. These genes include the dbpBA locus, whose products bind host decorin and glycosoaminoglycans. Recently, the dbpBA genes were reported to be involved in borrelial infectivity. Here we extended the previous observations by using culture and quantitative PCR to evaluate low- and high-dose murine infection by a {Delta}dbpBA::Gentr derivative of B. burgdorferi strain B31. The results indicate that the {Delta}dbpBA::Gentr mutant is attenuated in the ability to initially colonize and then persist in multiple tissues. The mutant exhibited a colonization defect as early as 3 days postinfection, before the development of an adaptive immune response, and after low-dose infection of SCID mice, which are deficient in adaptive immunity. These findings suggest that the inability to adhere to host decorin may promote clearance of B. burgdorferi, presumably via innate immune mechanisms. In a high-dose infection, the mutant disseminated to several tissues, particularly joint tissue, but it was generally cleared from these tissues by 3 weeks postinfection. Finally, following high-dose infection of SCID mice, the dbpBA mutant exhibited only a mild colonization defect, suggesting that the adaptive response is involved in the clearance of the mutant in immunocompetent mice. Taken together, these results suggest that the DbpBA proteins facilitate the colonization of multiple tissues by B. burgdorferi and are required for optimal resistance to both innate and adaptive immune mechanisms following needle inoculation.

* Corresponding author. Mailing address: 407 Reynolds Medical Building, Department of Microbial and Molecular Pathogenesis, Texas A&M Health Science Center, College Station, TX 77843. Phone: (979) 845-1376. Fax: (979) 845-3479. E-mail: jskare{at}medicine.tamhsc.edu

{triangledown} Published ahead of print on 22 September 2008.

Editor: J. B. Bliska

Infection and Immunity, December 2008, p. 5694-5705, Vol. 76, No. 12
0019-9567/08/$08.00+0     doi:10.1128/IAI.00690-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

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  • Mulay, V. B., Caimano, M. J., Iyer, R., Dunham-Ems, S., Liveris, D., Petzke, M. M., Schwartz, I., Radolf, J. D. (2009). Borrelia burgdorferi bba74 Is Expressed Exclusively during Tick Feeding and Is Regulated by Both Arthropod- and Mammalian Host-Specific Signals. J. Bacteriol. 191: 2783-2794 [Abstract] [Full Text]  


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