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Updated: May 23, 2026
A Mouse Model for Pathogen-induced Chronic Inflammation at Local and Systemic Sites
Published on: August 8, 2014
Streptococcus cristatus ArcA interferes with Porphyromonas gingivalis pathogenicity in mice
Background And Objective:
Porphyromonas gingivalis has been implicated as one of the major pathogens in chronic periodontitis, an infectious disease affecting the majority of the adult population. We have previously demonstrated that a surface protein, arginine deiminase (ArcA), of Streptococcus cristatus represses production of P. gingivalis long fimbriae and interrupts the formation of P. gingivalis biofilms in vitro. Our in vivo studies have also shown that the distribution of P. gingivalis and S. cristatus in human subgingival plaque is negatively correlated. The objective of this study was to determine if S. cristatus ArcA inhibits P. gingivalis colonization and attenuates its subsequent pathogenesis in alveolar bone loss in the murine oral cavity.
Material And Methods:
A wild-type strain of S. cristatus (CC5A) and its arcA knockout mutant (ArcAE) were used as initial colonizers in the oral cavity of BALB/cByJ mice. Colonization of P. gingivalis on the existing S. cristatus biofilms was assessed by quantitative PCR, and P. gingivalis-induced alveolar bone loss was measured 6 wk after P. gingivalis infection.
Results:
The presence of S. cristatus CC5A, but not its arcA mutant, attenuated P. gingivalis colonization in the murine oral cavity. In addition, P. gingivalis-induced alveolar bone loss was significantly lower in mice initially infected with S. cristatus CC5A than in those infected with the arcA mutant.
Conclusion:
This study provides direct evidence that S. cristatus ArcA has an inhibitory effect on P. gingivalis colonization, which may in turn attenuate the pathogenicity of P. gingivalis.
