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Infection and Immunity, February 2002, p. 491-497, Vol. 70, No. 2
0019-9567/01/$04.00+0     DOI: 10.1128/IAI.70.2.491-497.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.

Differential Binding of Host Complement Inhibitor Factor H by Borrelia burgdorferi Erp Surface Proteins: a Possible Mechanism Underlying the Expansive Host Range of Lyme Disease Spirochetes

Brian Stevenson,* Nazira El-Hage, Melissa A. Hines, Jennifer C. Miller, and Kelly Babb

Department of Microbiology and Immunology, University of Kentucky College of Medicine, Lexington, Kentucky 40536-0298

Received 21 August 2001/ Returned for modification 4 October 2001/ Accepted 22 October 2001

The Lyme disease spirochete, Borrelia burgdorferi, is capable of infecting a wide variety of vertebrates. This broad host range implies that B. burgdorferi possesses the ability to contravene the immune defenses of many potential hosts. B. burgdorferi produces multiple different Erp proteins on its outer membrane during mammalian infection. It was reported previously that one Erp protein can bind human factor H (J. Hellwage, T. Meri, T. Heikkilä, A. Alitalo, J. Panelius, P. Lahdenne, I. J. T. Seppälä, and S. Meri, J. Biol. Chem. 276:8427–8435, 2001). In this paper we report that the ability to bind the complement inhibitor factor H is a general characteristic of Erp proteins. Furthermore, each Erp protein exhibits different relative affinities for the complement inhibitors of various potential animal hosts. The data suggest that the presence of multiple Erp proteins on the surface can allow a single B. burgdorferi bacterium to resist complement-mediated killing in any of the wide range of potential hosts that it might infect. Thus, Erp proteins likely contribute to the persistence of B. burgdorferi in nature and to the ability of this bacterium to cause Lyme disease in humans and other animals.

* Corresponding author. Mailing address: Department of Microbiology and Immunology, University of Kentucky College of Medicine, MS 415 Chandler Medical Center, Lexington, KY 40536-0298. Phone: (859) 257-9358. Fax: (859) 257-8994. E-mail: bstev0{at}uky.edu.

Editor: D. L. Burns

Infection and Immunity, February 2002, p. 491-497, Vol. 70, No. 2
0019-9567/01/$04.00+0     DOI: 10.1128/IAI.70.2.491-497.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.



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