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The regulation of the kallikrein-kinin system is an important mechanism controlling vasodilation and promoting inflammation. We aimed to investigate the role of Toll-like receptor 2 (TLR2) in regulating kinin B 1  and B 2  receptor expression in human gingival fibroblasts and in mouse gingiva. Both  P. gingivalis  LPS and the synthetic TLR2 agonist Pam 2 CSK 4  increased kinin receptor transcripts. Silencing of TLR2, but not of TLR4, inhibited the induction of kinin receptor transcripts by both  P. gingivalis  LPS and Pam 2 CSK 4 . Human gingival fibroblasts (HGF) exposed to Pam 2 CSK 4  increased binding sites for bradykinin (BK, B 2  receptor agonist) and des-Arg 10 -Lys-bradykinin (DALBK, B 1  receptor agonist). Pre-treatment of HGF for 24 h with Pam 2 CSK 4  resulted in increased PGE 2  release in response to BK and DALBK. The increase of B1 and B2 receptor transcripts by  P. gingivalis  LPS was not blocked by IL-1β neutralizing antibody; TNF-α blocking antibody did not affect B 1  receptor up-regulation, but partially blocked increase of B 2  receptor mRNA. Injection of  P. gingivalis  LPS in mouse gingiva induced an increase of B 1  and B 2  receptor mRNA. These data show that activation of TLR2 in human gingival fibroblasts as well as in mouse gingival tissue leads to increase of B 1  and B 2  receptor mRNA and protein.

Activation of Toll-like receptor 2 induces B1 and B2 kinin receptors in human gingival fibroblasts and in mouse gingiva