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Department of Veterinary and Biomedical Sciences, Pennsylvania State University, 115 Henning Building, University Park, PA 16802, Graduate Program in Immunology and Infectious Diseases, Graduate Program in Pathobiology, Center for Biologics Evaluation and Research, FDA, 29 Lincoln Drive, Bethesda MD, 20892
* To whom correspondence should be addressed. Email: eth10{at}psu.edu.
| Abstract |
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Bordetella pertussis, a causative agent of whooping cough, expresses BrkA which confers serum resistance, but the closely related human pathogen that also causes whooping cough, B. parapertussis, does not. Interestingly, B. parapertussis, but not B. pertussis, produces an O-antigen, a factor shown in other models to confer serum resistance. Using a murine model of infection, we determined that O-antigen contributes to the ability of B. parapertussis to colonize the respiratory tract during the first week of infection, but not thereafter. Interestingly, an O-antigen deficient strain of B. parapertussis was not defective in colonizing mice lacking the complement cascade. O-antigen prevented both complement component C3 deposition on the surface, and complement mediated killing of B. parapertussis. In addition, O-antigen was required for B. parapertussis to systemically spread in complement-sufficient mice, but not complement-deficient mice. These data indicate that O-antigen enables B. parapertussis to efficiently colonize the lower respiratory tract by protecting against complement-mediated control and clearance.
| J. Bacteriol. | J. Virol. | Eukaryot. Cell |
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| Microbiol. Mol. Biol. Rev. | Clin. Vaccine Immunol. | All ASM Journals |
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