title: The role of RgpA in the pathogenicity of Porphyromonas gingivalis in the murine periodontitis model.
abstract: OBJECTIVE
  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.
  
  
  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.
authors.affiliation: Department of Periodontology, School of Dental Medicine, Hebrew University and Hadassah, Jesusalem, Israel.
authors.forename: Asaf
authors.initials: A
authors.lastname: Wilensky
authors.forename: David
authors.initials: D
authors.lastname: Polak
authors.forename: Yael
authors.initials: Y
authors.lastname: Houri-Haddad
authors.forename: Lior
authors.initials: L
authors.lastname: Shapira
mesh_terms: D018829:Adhesins, Bacterial / Q000502:physiology*; D016301:Alveolar Bone Loss / Q000276:immunology / Q000382:microbiology; D000818:Animals; D000907:Antibodies, Bacterial / Q000097:blood; D058491:Bacterial Load; D016866:Bacteroidaceae Infections / Q000276:immunology / Q000382:microbiology; D003546:Cysteine Endopeptidases / Q000502:physiology*; D015194:Diffusion Chambers, Culture; D004195:Disease Models, Animal; D005260:Female; D000080867:Gingipain Cysteine Endopeptidases; D007074:Immunoglobulin G / Q000097:blood; D016753:Interleukin-10 / Q000032:analysis; D053583:Interleukin-1beta / Q000032:analysis; D007958:Leukocyte Count; D051379:Mice; D008807:Mice, Inbred BALB C; D050296:Microbial Viability; D010518:Periodontitis / Q000276:immunology / Q000382:microbiology*; D010587:Phagocytosis / Q000502:physiology; D016966:Porphyromonas gingivalis / Q000201:enzymology / Q000276:immunology / Q000472:pathogenicity*; D013047:Specific Pathogen-Free Organisms; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis; D014774:Virulence; D037521:Virulence Factors / Q000502:physiology*; D055114:X-Ray Microtomography / Q000379:methods
chemical_list: D018829:Adhesins, Bacterial; D000907:Antibodies, Bacterial; D000080867:Gingipain Cysteine Endopeptidases; C556062:IL10 protein, mouse; D007074:Immunoglobulin G; D053583:Interleukin-1beta; D014409:Tumor Necrosis Factor-alpha; D037521:Virulence Factors; D016753:Interleukin-10; D003546:Cysteine Endopeptidases
keywords: Porphyromonas gingivalis; alveolar bone loss; cytokines; experimental periodontitis; immunoglobulins; phagocytosis