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Infection and Immunity, June 2007, p. 2786-2794, Vol. 75, No. 6
0019-9567/07/$08.00+0     doi:10.1128/IAI.01307-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Infection of Mice with Lyme Disease Spirochetes Constitutively Producing Outer Surface Proteins A and B{triangledown}

Keith O. Strother,1 Emir Hodzic,2 Stephen W. Barthold,2 and Aravinda M. de Silva1*

Department of Microbiology and Immunology, 720 Mary Ellen Jones Building, CB 7290, University of Chapel Hill, Chapel Hill, North Carolina, 27599,1 Center for Comparative Medicine, University of California, Davis, County Road 98 and Hutchison Drive, Davis, California 956162

Received 14 August 2006/ Returned for modification 27 September 2006/ Accepted 8 March 2007

Outer surface protein A (OspA) of the Lyme disease spirochete is primarily produced in the tick vector. OspA, which is a receptor for attaching spirochetes to the tick gut, is down regulated as the spirochetes leave the tick and enter the mammalian host. Although OspA is not a major antigen produced in the mammal, the protein appears to be produced under some conditions and production has been linked to more severe disease. A Lyme disease vaccine based on recombinant OspA has been approved for human use. However, the vaccine is no longer available, in part because of fears that OspA causes arthritis in people. To further understand the consequences of OspA production in the host, we created a Borrelia burgdorferi mutant that was unable to down regulate OspA. C3H/HeN mice infected with this mutant developed a specific anti-OspA immune response, and the spirochetes were unable to persist in these mice. In contrast, immunodeficient SCID mice were persistently infected with the mutant. We conclude that spirochetes producing OspA and B from the flaB promoter in immunocompetent mice stimulate an immune response that clear the bacteria without any signs of disease development in the mice.

* Corresponding author. Mailing address: Department of Microbiology and Immunology, 720 Mary Ellen Jones Building, CB 7290, University of Chapel Hill, Chapel Hill, NC 27599. Phone: (919) 843-9964. Fax: (919) 962-8103. E-mail: desilva{at}med.unc.edu

{triangledown} Published ahead of print on 19 March 2007.

Editor: R. P. Morrison

Infection and Immunity, June 2007, p. 2786-2794, Vol. 75, No. 6
0019-9567/07/$08.00+0     doi:10.1128/IAI.01307-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Xu, Q., McShan, K., Liang, F. T. (2008). Modification of Borrelia burgdorferi to overproduce OspA or VlsE alters its infectious behaviour. Microbiology 154: 3420-3429 [Abstract] [Full Text]  
  • Xu, Q., Seemanaplli, S. V., McShan, K., Liang, F. T. (2007). Increasing the Interaction of Borrelia burgdorferi with Decorin Significantly Reduces the 50 Percent Infectious Dose and Severely Impairs Dissemination. Infect. Immun. 75: 4272-4281 [Abstract] [Full Text]  


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