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 Simmons, W. L.
Right arrow Articles by Dybvig, K.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Simmons, W. L.
Right arrow Articles by Dybvig, K.

 Previous Article  |  Next Article 

Infection and Immunity, December 2004, p. 6846-6851, Vol. 72, No. 12
0019-9567/04/$08.00+0     DOI: 10.1128/IAI.72.12.6846-6851.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

Resistance of Mycoplasma pulmonis to Complement Lysis Is Dependent on the Number of Vsa Tandem Repeats: Shield Hypothesis

Warren L. Simmons,1* Amy M. Denison,2 and Kevin Dybvig1

Departments of Genetics,1 Pathology, University of Alabama at Birmingham, Birmingham, Alabama2

Received 10 May 2004/ Returned for modification 15 July 2004/ Accepted 13 August 2004

The Vsa proteins are associated with the virulence of the murine respiratory pathogen Mycoplasma pulmonis. The antigens consist of a conserved N-terminal region that is combined with one of several different variable C-terminal regions comprised of tandem repeats. M. pulmonis strains that produce VsaA with about 40 tandem repeats do not adhere to polystyrene or erythrocytes and are highly resistant to complement killing. Strains that produce VsaA with three tandem repeats adhere strongly to polystyrene and erythrocytes and are highly susceptible to complement killing. We report here that the resistance to complement lysis was not due to a lack of activation of the complement cascade. Isolation and analysis of M. pulmonis strains that produced Vsa proteins other than VsaA (VsaG and VsaI) with either long or short repeat regions indicated that adherence to polystyrene and resistance to complement were dependent on the length of the repeat region but not on the Vsa type. Furthermore, M. pulmonis Vsa variants were susceptible to the polypeptide pore-forming molecule gramicidin D, independent of the Vsa type and length. Collectively, the data indicate the Vsa proteins nonspecifically mediate M. pulmonis surface interactions and function to sterically hinder access of complement to the mycoplasma cell membrane while permitting access of smaller molecules.

* Corresponding author. Mailing address: Department of Genetics, University of Alabama at Birmingham, 720 South 20th Street, Kaul Room 720, Birmingham, AL 35294-0024. Phone: (205) 934-2794. Fax: (205) 975-4418. E-mail: wsimmons{at}uab.edu.

Editor: J. T. Barbieri

Infection and Immunity, December 2004, p. 6846-6851, Vol. 72, No. 12
0019-9567/04/$08.00+0     DOI: 10.1128/IAI.72.12.6846-6851.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Nouvel, L.-X., Marenda, M., Sirand-Pugnet, P., Sagne, E., Glew, M., Mangenot, S., Barbe, V., Barre, A., Claverol, S., Citti, C. (2009). Occurrence, Plasticity, and Evolution of the vpma Gene Family, a Genetic System Devoted to High-Frequency Surface Variation in Mycoplasma agalactiae. J. Bacteriol. 191: 4111-4121 [Abstract] [Full Text]  
  • Simmons, W. L., Dybvig, K. (2007). Biofilms Protect Mycoplasma pulmonis Cells from Lytic Effects of Complement and Gramicidin. Infect. Immun. 75: 3696-3699 [Abstract] [Full Text]  
  • Simmons, W. L., Bolland, J. R., Daubenspeck, J. M., Dybvig, K. (2007). A Stochastic Mechanism for Biofilm Formation by Mycoplasma pulmonis. J. Bacteriol. 189: 1905-1913 [Abstract] [Full Text]  
  • Wise, K. S., Foecking, M. F., Roske, K., Lee, Y. J., Lee, Y. M., Madan, A., Calcutt, M. J. (2006). Distinctive Repertoire of Contingency Genes Conferring Mutation- Based Phase Variation and Combinatorial Expression of Surface Lipoproteins in Mycoplasma capricolum subsp. capricolum of the Mycoplasma mycoides Phylogenetic Cluster. J. Bacteriol. 188: 4926-4941 [Abstract] [Full Text]  
  • Mrazek, J. (2006). Analysis of Distribution Indicates Diverse Functions of Simple Sequence Repeats in Mycoplasma Genomes. Mol Biol Evol 23: 1370-1385 [Abstract] [Full Text]  
  • Fehri, L. F., Sirand-Pugnet, P., Gourgues, G., Jan, G., Wroblewski, H., Blanchard, A. (2005). Resistance to Antimicrobial Peptides and Stress Response in Mycoplasma pulmonis. Antimicrob. Agents Chemother. 49: 4154-4165 [Abstract] [Full Text]  
  • Denison, A. M., Clapper, B., Dybvig, K. (2005). Avoidance of the Host Immune System through Phase Variation in Mycoplasma pulmonis. Infect. Immun. 73: 2033-2039 [Abstract] [Full Text]  


Copyright © 2009 by the American Society for Microbiology.   For an alternate route to Journals.ASM.org, visit: http://intl-journals.asm.org | More Info»