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Infect. Immun. doi:10.1128/IAI.01923-06
Copyright (c) 2007, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.

Borrelia burgdorferi binding of host complement regulator factor H is not required for efficient mammalian infection

Department of Microbiology, Immunology, and Molecular Genetics, University of Kentucky College of Medicine, Lexington, KY 40536; Department of Medical Microbiology and Immunology, University of Toledo Health Sciences Campus, Toledo, OH 43614; Washington D.C. 20036; Molecular Genetics and Rheumatology Section, Division of Medicine, Imperial College, Hammersmith Campus, London W12 0NN, United Kingdom; Leibniz-Institute for Natural Products Research and Infection Biology/Hans Knöll Institute, Beutenbergstrasse 11a, D-07745 Jena, Germany

^* To whom correspondence should be addressed. Email: brian.stevenson{at}uky.edu.

	Abstract

The causative agent of Lyme disease, Borrelia burgdorferi, is naturally resistant to its hosts' alternative pathway of complement-mediated killing. Several different borrelial outer surface proteins have been identified as being able to bind host factor H, a regulator of the alternative pathway, leading to a hypothesis that such binding is important for borrelial resistance to complement. To test this hypothesis, the development of B. burgdorferi infection was compared between factor H-deficient and wild-type mice. Factor B- and C3-deficient mice were also studied to determine the relative roles of the alternative and classical/lectin pathways on B. burgdorferi survival during mammalian infection. While it was predicted that B. burgdorferi should be impaired in its ability to infect factor H-deficient animals, quantitiative analyses of bacterial loads indicated that those mice were infected at levels similar to wild-type, factor B- and C3-deficient mice. Ticks fed on infected factor H-deficient or wild-type mice all acquired similar numbers of bacteria. Indirect immunofluorescence analysis of B. burgdorferi acquired by feeding ticks from the blood of infected mice indicated that none of the bacteria had detectable levels of factor H on their outer surfaces, even though such bacteria express high levels of surface proteins capable of binding factor H. These findings demonstrate that acquisition of host factor H is not essential for mammalian infection by B. burgdorferi, and indicate that additional mechanisms are employed by the Lyme disease spirochete to evade complement-mediated killing.

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