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Infection and Immunity, March 2007, p. 1436-1442, Vol. 75, No. 3
0019-9567/07/$08.00+0     doi:10.1128/IAI.01627-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Kgp and RgpB, but Not RgpA, Are Important for Porphyromonas gingivalis Virulence in the Murine Periodontitis Model{triangledown}

Rishi D. Pathirana, Neil M. O'Brien-Simpson, Gail C. Brammar, Nada Slakeski, and Eric C. Reynolds*

Cooperative Research Centre for Oral Health Science, School of Dental Science, and the Bio21 Institute of Molecular Science and Biotechnology, The University of Melbourne, Melbourne, Victoria, Australia

Received 8 October 2006/ Returned for modification 28 November 2006/ Accepted 21 December 2006

The contributions of three proteinase genes (rgpA, rgpB, and kgp) to the virulence of Porphyromonas gingivalis W50 were investigated in the murine periodontitis model. Mice were orally inoculated with eight doses (1 x 1010 cells per dose) of rgpA, rgpB, kgp, rgpA rgpB, or rgpA rgpB kgp isogenic mutants, and the level of alveolar bone loss, immune response induced, and number of bacterial cells per half maxilla were compared with those of animals inoculated with wild-type P. gingivalis. The kgp, rgpB, rgpA rgpB, and rgpA rgpB kgp isogenic mutants induced significantly (P < 0.05) less bone loss than the rgpA isogenic mutant and the wild type did, and the virulence of the rgpA isogenic mutant and the wild type were not significantly different. Mice inoculated with the wild type or the rgpA isogenic mutant exhibited significantly (P < 0.01) more P. gingivalis cells per half maxilla than mice inoculated with rgpB, kgp, rgpA rgpB, and rgpA rgpB kgp isogenic mutants or nonchallenged mice did, as determined using real-time PCR. A significant positive correlation was found between the number of P. gingivalis cells detected per half maxilla and the amount of alveolar bone loss induced. Enzyme-linked immunosorbent assay results showed that each isogenic mutant and the wild type induced a predominant P. gingivalis antigen-specific immunoglobulin G3 (IgG3) response. Furthermore, the kgp and rgpA rgpB kgp isogenic mutants induced significantly (P < 0.05) lower IgG3 antibody responses than the responses induced by the wild type or the rgpA, rgpB, and rgpA rgpB isogenic mutants. The results suggest that the order in which the proteinases contribute to the virulence of P. gingivalis in the murine periodontitis model is Kgp ≥ RgpB >> RgpA.


* Corresponding author. Mailing address: Centre for Oral Health Science, School of Dental Science, Faculty of Medicine, Dentistry and Health Sciences, The University of Melbourne, 720 Swanston Street, Melbourne, Victoria 3010, Australia. Phone: 61 3 9341 1547. Fax: 61 3 9341 1596. E-mail: e.reynolds{at}unimelb.edu.au.

{triangledown} Published ahead of print on 12 January 2007.

Editor: A. D. O'Brien


Infection and Immunity, March 2007, p. 1436-1442, Vol. 75, No. 3
0019-9567/07/$08.00+0     doi:10.1128/IAI.01627-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.




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