Streptococcus cristatus ArcA interferes with Porphyromonas gingivalis pathogenicity in mice

Abstract

Xie H, Hong J, Sharma A, Wang B‐Y. Streptococcus cristatus ArcA interferes with Porphyromonas gingivalis pathogenicity in mice. J Periodont Res 2012; 47: 578–583. © 2012 John Wiley & Sons A/S 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.

Porphyromonas gingivalisdisturbs host–commensal homeostasis by changing complement function

“…For instance, Streptococcus cristatus inhibits fimbrial gene expression in P. gingivalis through the signaling action of arginine deiminase [76]. Consistent with this finding, in human subgingival plaque, the distribution of the two organisms is negatively correlated [77]. Moreover, S. cristatus suppresses P. gingivalis –induced alveolar bone loss in a mouse model [77].…”

Polymicrobial synergy and dysbiosis in inflammatory disease

“…S. cristatus for example, induces downregulation of fimbrial gene expression in P. gingivalis through the signaling action of arginine deiminase [34]. Consequently, the distribution of P. gingivalis and S. cristatus in human subgingival plaque is negatively correlated, and S. cristatus attenuates P. gingivalis -induced bone loss in mice [35]. Such antagonistic interaction may lead to a ‘Red Queen’ effect, as P. gingivalis can induce cell death of another oral streptococcus, S. mitis [18].…”

Lipopolysaccharides-Induced Suppression of Innate-Like B Cell Apoptosis Is Enhanced by CpG Oligodeoxynucleotide and Requires Toll-Like Receptors 2 and 4

“…These unconventional B cells with autoreactive properties can provide a rapid T cell-independent antibody response to protect against infections [15]. Innate-like B cells in mice are composed of B1 cells [16], marginal zone (MZ) B cells [17] and other related B cells [18]. Recent studies indicated that innate-like B cells can link innate immunity to adaptive immune responses during infection [19, 20].…”