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The role of RgpA in the pathogenicity of Porphyromonas gingivalis in the murine periodontitis model
Author(s) -
Wilensky Asaf,
Polak David,
HouriHaddad Yael,
Shapira Lior
Publication year - 2013
Publication title -
journal of clinical periodontology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.456
H-Index - 151
eISSN - 1600-051X
pISSN - 0303-6979
DOI - 10.1111/jcpe.12139
Subject(s) - porphyromonas gingivalis , periodontitis , microbiology and biotechnology , virulence , phagocytosis , dental alveolus , in vivo , virulence factor , proteases , inflammation , chemistry , immunology , biology , medicine , biochemistry , dentistry , gene , enzyme
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.