Porphyromonas gingivalis promotes neointimal formation after arterial injury through toll-like receptor 2 signaling.

We previously demonstrated that Porphyromonas gingivalis infection induces neointimal hyperplasia with an increase in monocyte chemoattractant protein (MCP)-1 after arterial injury in wild-type mice. Toll-like receptor (TLR) 2 is a key receptor for the virulence factors of P. gingivalis. The aim of this study was to assess whether TLR2 plays a role in periodontopathic bacteria-induced neointimal formation after an arterial injury. Wild-type and TLR2-deficient mice were used in this study. The femoral arteries were injured, and P. gingivalis or vehicle was injected subcutaneously once per week. Fourteen days after arterial injury, the murine femoral arteries were obtained for histopathologic and immunohistochemical analyses. The immunoglobulin-G levels of the P. gingivalis-infected groups were significantly increased in comparison with the level in the corresponding noninfected groups in both wild-type and TLR2-deficient mice. TLR2 deficiency negated the P. gingivalis-induced neointimal formation in comparison with the wild-type mice, and reduced the number of positive monocyte chemoattractant protein-1 cells in the neointimal area. These findings demonstrate that P. gingivalis infection can promote neointimal formation after an arterial injury through TLR2 signaling.