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Borrelia burgdorferiBinding of Host Complement Regulator Factor H Is Not Required for Efficient Mammalian Infection
Author(s) -
Michael E. Woodman,
Anne Cooley,
Jennifer C. Miller,
John J. Lazarus,
Kathryn Tucker,
Tomasz Bykowski,
Marina Botto,
Jens Hellwage,
R. Mark Wooten,
Brian Stevenson
Publication year - 2007
Publication title -
infection and immunity
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.508
H-Index - 220
eISSN - 1070-6313
pISSN - 0019-9567
DOI - 10.1128/iai.01923-06
Subject(s) - borrelia burgdorferi , biology , borrelia , regulator , microbiology and biotechnology , factor h , host (biology) , complement system , complement (music) , virology , host factor , spirochaetaceae , immunology , antibody , genetics , virus , complementation , gene , phenotype
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 ofB. 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 inB. burgdorferi survival during mammalian infection. While it was predicted thatB. 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 ofB. 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 byB. burgdorferi and indicate that additional mechanisms are employed by the Lyme disease spirochete to evade complement-mediated killing.

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