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Infection and Immunity, September 2003, p. 4936-4942, Vol. 71, No. 9
0019-9567/03/$08.00+0 DOI: 10.1128/IAI.71.9.4936-4942.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.
Christina S. Hutter,
and Eric T. Harvill*
Department of Veterinary Science, The Pennsylvania State University, University Park, Pennsylvania
Received 28 March 2003/ Returned for modification 8 May 2003/ Accepted 11 June 2003
In order to initially colonize a host, bacteria must avoid various components of the innate immune system, one of which is complement. The genus Bordetella includes three closely related species that differ in their ability to resist complement-mediated killing. Bordetella parapertussis and Bordetella bronchiseptica resist killing in naïve serum, a characteristic that may aid in efficient respiratory tract colonization and has been attributed to expression of O antigen. Bordetella pertussis lacks O antigen and is sensitive to naïve serum in vitro, yet it also efficiently colonizes the respiratory tract. Based on these observations, we hypothesized that B. pertussis may have an alternate mechanism to resist complement in vivo. While a number of reports on serum sensitivity of the bordetellae have been published, we show here that serum concentration and growth conditions can greatly alter the observed level of sensitivity to complement and that all but one strain of B. pertussis observed were sensitive to some level of naïve serum in vitro, particularly when there was excess complement. However, B. pertussis rapidly acquires increased resistance in vivo to naïve serum that is specific to the alternative pathway. Resistance is not efficiently acquired by B. parapertussis and B. bronchiseptica mutants lacking O antigen. This B. pertussis-specific mechanism of complement resistance does not appear to be dependent on either brkA or other genes expressed specifically in the Bvg+ phase. This in vivo acquisition of alternative pathway resistance suggests that there is a novel O antigen-independent method by which B. pertussis evades complement-mediated killing.
Present address: Department of Medicine, Division of Hematology/Oncology, University of California, Los Angeles, Center for the Health Sciences, Los Angeles, CA 90095-1678.
Present address: Cold Spring Harbor Laboratory, Cold Spring Harbor, NY 11724.
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