Activation of local innate immune signal induces periodontitis in microbiota-dependent manner.
Periodontitis is a chronic inflammatory disease. Both inflammation and dysbiosis have been implicated in periodontitis development. However, the relationship between local inflammation and dysbiosis, and the precise roles of local inflammation in periodontitis are not well-elucidated. In present study, we explored the role of local inflammation in periodontitis. We established a periodontitis model by administration of Pam3CSK4 to local oral area and compared the difference of outcome between local and systemic administration. We monitored the pro-inflammatory cytokine expression, local inflammation and alveolar bone loss. We also evaluated the dysbiosis, NF-κB activation. Local but not systemic administration of Pam3CSK4-induced pro-inflammatory cytokines productions and finally resulted in periodontitis. Pam3CSK4 caused dysbiosis and promoted Porphyromonas gingivalis growth. The bacterial growth and NF-κB activation were required for Pam3CSK4-induced periodontitis. We evaluated the effect of local inflammation by inducing TLR2 activation on dysbiosis and periodontitis. Activation of local innate immune signal induces periodontitis in microbiota-dependent manner.
['Wang|Nan|N|', 'Xia|Dengsheng|D|']
D000818:Animals D016866:Bacteroidaceae Infections D006801:Humans D007113:Immunity, Innate D007249:Inflammation D018836:Inflammation Mediators D064307:Microbiota D016328:NF-kappa B D010518:Periodontitis D016966:Porphyromonas gingivalis D015398:Signal Transduction
periodontitis Pam3CSK4 NF-κB innate immune response microbiota