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Infection and Immunity, June 2007, p. 3131-3139, Vol. 75, No. 6
0019-9567/07/$08.00+0     doi:10.1128/IAI.01923-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Borrelia burgdorferi Binding of Host Complement Regulator Factor H Is Not Required for Efficient Mammalian Infection{triangledown}

Michael E. Woodman,1 Anne E. Cooley,1 Jennifer C. Miller,1,{dagger} John J. Lazarus,2 Kathryn Tucker,3 Tomasz Bykowski,1 Marina Botto,4 Jens Hellwage,5,{ddagger} R. Mark Wooten,2 and Brian Stevenson1*

Department of Microbiology, Immunology, and Molecular Genetics, University of Kentucky College of Medicine, Lexington, Kentucky 40536,1 Department of Medical Microbiology and Immunology, University of Toledo Health Sciences Campus, Toledo, Ohio 43614,2 Statistics Collaborative, Inc., Washington, DC 20036,3 Molecular Genetics and Rheumatology Section, Division of Medicine, Imperial College, Hammersmith Campus, London W12 0NN, United Kingdom,4 Leibniz Institute for Natural Products Research and Infection Biology, Hans Knöll Institute, Beutenbergstrasse 11a, D-07745 Jena, Germany5

Received 5 December 2006/ Returned for modification 12 March 2007/ Accepted 27 March 2007

The causative agent of Lyme disease, Borrelia burgdorferi, is naturally resistant to its host's 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 in 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, quantitative analyses of bacterial loads indicated that those mice were infected at levels similar to those of wild-type and 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 the 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.

* Corresponding author. Mailing address: Department of Microbiology, Immunology, and Molecular Genetics, University of Kentucky College of Medicine, MS421 W. R. Willard Medical Education Building, Lexington, KY 40536-0298. Phone: (859) 257-9358. Fax: (859) 257-8994. E-mail: brian.stevenson{at}uky.edu

{triangledown} Published ahead of print on 9 April 2007.

Editor: A. D. O'Brien

{dagger} Present address: Department of Pathology, University of Utah, Salt Lake City, UT 84132.

{ddagger} Present address: 4-Antibody AG, Winzerlaer Strasse 2, D-07745 Jena, Germany.

Infection and Immunity, June 2007, p. 3131-3139, Vol. 75, No. 6
0019-9567/07/$08.00+0     doi:10.1128/IAI.01923-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.



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