IADR Abstract Archives
Metronidazole-Treated Porphyromonas Gingivalis Persistent Cells Suppress Immuno-Inflammatory Response in Hgecs
Objectives: This study aimed to investigate the effects of Porphyromonas gingivalis on the immuno-inflammatory response in human gingival epithelial cells.
Methods: Primary human gingival epithelial cells (HGECs) were pre-treated with IL-1β for 24 hours. P. gingivalis cells (ATCC 33277) were cultured anaerobically to stationary phase followed by treatment with lethal doses of metronidazole (MTZ) for 6 hours. Then, the HGECs with or without IL-1β pre-treatment were stimulated with MTZ-treated or live P. gingivalis as well as heat-killed MTZ-treated or live P. gingivalis for 6 hours. The expression levels of pro-inflammatory cytokines IL-6 and IL-8 were detected by ELISA and qPCR.
Results: The expression of IL-6 and IL-8 in HGECs was enhanced dramatically by IL-1β after 24 hours. Live and heat-killed P. gingivalis had little effects on the expression of both IL-6 and IL-8 in HGECs, so did MTZ-treated or heat-killed MTZ-treated P. gingivalis persistent cells. The IL-1β-upregulated expression of IL-6 and IL-8 was significantly suppressed by live P. gingivalis at both RNA and protein levels, and notably, MTZ-treated P. gingivalis persistent cells showed similar inhibiting effect. However, heat-killed P. gingivalis or heat-killed MTZ-treated P. gingivalis persistent cells could not significantly suppress IL-1β induced expression of IL-6 and IL-8.
Conclusions: The present findings suggest that P. gingivalis may critically enhance its persistent survival under harsh environmental condition through suppressing immuno-inflammatory response, thereby contributing to periodontal pathogenesis.
Methods: Primary human gingival epithelial cells (HGECs) were pre-treated with IL-1β for 24 hours. P. gingivalis cells (ATCC 33277) were cultured anaerobically to stationary phase followed by treatment with lethal doses of metronidazole (MTZ) for 6 hours. Then, the HGECs with or without IL-1β pre-treatment were stimulated with MTZ-treated or live P. gingivalis as well as heat-killed MTZ-treated or live P. gingivalis for 6 hours. The expression levels of pro-inflammatory cytokines IL-6 and IL-8 were detected by ELISA and qPCR.
Results: The expression of IL-6 and IL-8 in HGECs was enhanced dramatically by IL-1β after 24 hours. Live and heat-killed P. gingivalis had little effects on the expression of both IL-6 and IL-8 in HGECs, so did MTZ-treated or heat-killed MTZ-treated P. gingivalis persistent cells. The IL-1β-upregulated expression of IL-6 and IL-8 was significantly suppressed by live P. gingivalis at both RNA and protein levels, and notably, MTZ-treated P. gingivalis persistent cells showed similar inhibiting effect. However, heat-killed P. gingivalis or heat-killed MTZ-treated P. gingivalis persistent cells could not significantly suppress IL-1β induced expression of IL-6 and IL-8.
Conclusions: The present findings suggest that P. gingivalis may critically enhance its persistent survival under harsh environmental condition through suppressing immuno-inflammatory response, thereby contributing to periodontal pathogenesis.