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Infection and Immunity, January 2002, p. 403-406, Vol. 70, No. 1
0019-9567/01/$04.00+0 DOI: 10.1128/IAI.70.1.403-406.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.
Department of Molecular Genetics, Biochemistry and Microbiology, University of Cincinnati, Cincinnati, Ohio 45267
Received 11 July 2001/ Returned for modification 4 September 2001/ Accepted 26 September 2001
The BrkA protein of Bordetella pertussis inhibits killing by the antibody-dependent classical pathway of complement; however, susceptibility to complement can be highly variable. Log-phase bacteria grown in Stainer-Scholte (SS) broth plated on Bordet-Gengou (BG) agar were about 500 times more sensitive to killing by complement than stationary-phase SS-BG cultures. While always more susceptible to complement than the wild-type strain, a BrkA mutant displayed a similar growth phase variation in susceptibility to complement. Growth phase susceptibility to complement was also observed for a mutant constitutive for Bvg activation of BrkA, suggesting that modulation of virulence factor expression was not responsible for sensitivity to complement. Susceptibility was not due to differential antigenic expression, since serum adsorbed with complement-resistant, stationary-phase SS-BG cultures lacked bactericidal activity against B. pertussis harvested at all times during the growth cycle. These results suggest that log-phase susceptibility to complement is not due to variable expression of BrkA or antigenic differences and may be an inherent property of rapidly growing cultures. Implications for vaccine development are discussed.
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