This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowReprints and Permissions
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Barnes, M. G.
Right arrow Articles by Weiss, A. A.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Barnes, M. G.
Right arrow Articles by Weiss, A. A.

 Previous Article  |  Next Article 

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.

Growth Phase Influences Complement Resistance of Bordetella pertussis

Michael G. Barnes and Alison A. Weiss*

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.


* Corresponding author. Mailing address: Department of Molecular Genetics, Biochemistry and Microbiology, University of Cincinnati, 231 Sabin Way, ML 0524, Cincinnati, OH 45267. Phone: (513) 558-2820. Fax: (513) 558-8474. E-mail: Alison.Weiss{at}uc.edu.

Editor: D. L. Burns


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.




This article has been cited by other articles:

  • Aase, A., Herstad, T. K., Merino, S., Brandsdal, K. T., Berdal, B. P., Aleksandersen, E. M., Aaberge, I. S. (2007). Opsonophagocytic Activity and Other Serological Indications of Bordetella pertussis Infection in Military Recruits in Norway. CVI 14: 855-862 [Abstract] [Full Text]  
  • Kristian, S. A., Timmer, A. M., Liu, G. Y., Lauth, X., Sal-Man, N., Rosenfeld, Y., Shai, Y., Gallo, R. L., Nizet, V. (2007). Impairment of innate immune killing mechanisms by bacteriostatic antibiotics. FASEB J. 21: 1107-1116 [Abstract] [Full Text]  
  • Pishko, E. J., Betting, D. J., Hutter, C. S., Harvill, E. T. (2003). Bordetella pertussis Acquires Resistance to Complement-Mediated Killing In Vivo. Infect. Immun. 71: 4936-4942 [Abstract] [Full Text]