Porphyromonas gingivalis promotes the cell cycle and inflammatory cytokine production in periodontal ligament fibroblasts

• We established the model of P. gingivalis infected human primary PDLFs.
• P. gingivalis enhanced the proliferation and G1 phase of PDLFs.
• P. gingivalis induced the decrease of p21 and increase of cyclin D1 and cyclin E.
• P. gingivalis promoted the expressions of IL-6 and IL-8 of PDLFs.

ObjectiveThe infection of Porphyromonas gingivalis (P. gingivalis) modulates host immune-inflammatory responses and destructs homeostasis of normal cell cycle, thereby leading to periodontal tissue destruction. Human periodontal ligament fibroblasts (PDLFs) are key players in the host immune responses and periodontal tissue regeneration. The aim of the present study was to discover the effects of P. gingivalis infection on the cell cycle and inflammatory cytokine production in PDLFs.DesignP. gingivalis infection model into PDLFs was established. The effect of P. gingivalis on the cell proliferation and cell cycle were detected by MTT and flow cytometry. The p21, cyclin D1 and cyclin E mRNA expression, p21 protein expression, as well as IL-6 and IL-8 protein levels were analyzed by RT-qPCR, Western blot and ELISA, respectively.ResultsP. gingivalis promoted proliferation and G1 phase of PDLFs. G1 phase promotion was associated with the decreased level of p21 and the up-regulation of cyclin D1 at 6 h, and with the increased level of cyclin E at 12 h. Simultaneously, the immune-inflammatory response of PDLFs was initiated by P. gingivalis during the initial stage of infection, including the increased expressions of IL-6 and IL-8.ConclusionWe confirmed that the infection of P. gingivalis could modulate the expression of PDLF genes, which control cell cycle and inflammatory cytokine production. Thus, P. gingivalis may contribute to the proliferation and inflammation of periodontal tissue.