The role of RgpA in the pathogenicity of Porphyromonas gingivalis in the murine periodontitis model

Authors

  • Asaf Wilensky,

    Corresponding author
    1. Department of Periodontology, School of Dental Medicine, Hebrew University and Hadassah, Jesusalem, Israel
    • Address:

      Asaf Wilensky Department of Periodontology, Dental Faculty, Hadassah and the Hebrew University Medical Center, P.O. Box 12272, Jerusalem 91120, Israel

      E-mail: asafw@ekmd.huji.ac.il

    Search for more papers by this author
  • David Polak,

    1. Department of Periodontology, School of Dental Medicine, Hebrew University and Hadassah, Jesusalem, Israel
    Search for more papers by this author
  • Yael Houri-Haddad,

    1. Department of Prosthodontics, School of Dental Medicine, Hebrew University and Hadassah, Jesusalem, Israel
    Search for more papers by this author
    • LS and YHH had equal contribution to the study.
  • Lior Shapira

    1. Department of Periodontology, School of Dental Medicine, Hebrew University and Hadassah, Jesusalem, Israel
    Search for more papers by this author
    • LS and YHH had equal contribution to the study.

  • Conflict of interest and source of funding statement

    The authors declare that they have no conflict of interests. This study was supported in part by the US-Israel Bi-National Science Foundation (US-Israel BSF).

Abstract

Aim

To investigate the in vivo role of gingipains in Porphyromonas gingivalis' virulence, and suggest a possible host mechanisms through which the bacteria cause alveolar bone loss.

Materials and Methods

Mice were orally infected with P. gingivalis wild type, or the gingipains mutants (RgpA, Kgp, RgpA/Kgp). Mice were analysed for alveolar bone loss using micro-computed tomography. The molecular effects of the proteases were evaluated using the subcutaneous chamber model. Mice were infected with P. gingivalis wild type or mutants. Exudates were analysed for cytokine and leukocytes levels, in vivo phagocytosis, P. gingivalis survival and serum anti-P. gingivalis IgG titres.

Results

Only RgpA-expressing bacteria induced significantly alveolar bone loss, and suppressed phagocytosis resulting in increased survival of P. gingivalis in the chamber exudates. In addition, RgpA-expressing bacteria induced higher levels of leukocytes and cytokines 2 h post-infection, and reduced levels of serum anti-P. gingivalis IgG titres 7 days post-infection.

Conclusions

Our findings showed that elimination of RgpA from P. gingivalis diminished inflammation, but augmented phagocytosis and antibody titres, coincidental with reduced alveolar bone loss. These findings support the hypothesis that RgpA is a critical virulence factor in the pathogenesis of experimental periodontitis in mice.

Ancillary