TNF receptor-associated factor 6 suppression inhibits inflammatory response to Porphyromonas gingivialis in human periodontal ligament cells.

OBJECTIVE

Periodontitis is a group of inflammatory diseases caused by microorganisms. Porphyromonas gingivalis, a gram-negative bacteria, is strongly associated with the onset of periodontitis. Tumor necrosis factor (TNF) receptor-associated factor 6 (TRAF6) represents an important target in the regulation of many disease processes, including immunity, inflammation, and osteoporosis. The aim of this study was to investigate the role of TRAF6 for inflammatory response in P gingivalis-infected human periodontal ligament cells (HPDLCs).

METHOD AND MATERIALS

HPDLCs were stimulated with 1 x 108 CFU/mL P gingivalis, or 10 ug/mL P gingivalis lipopolysaccharide (LPS), separately in the absence or presence of small interfering RNA (siRNA) for TRAF6. The expression of TRAF6 was examined by real-time polymerase chain reaction and Western blot analysis. Concentrations of IL-1B, IL-6, and IL-8 in the culture supernatants were determined by enzyme-linked immunosorbent assay (ELISA).

RESULTS

In this study, we found that both P gingivalis and its LPS treatment increased the expression of TRAF6 and proinflammatory cytokine production in HPDLCs. In addition, we used siRNA for TRAF6, and the inhibition of TRAF6 expression reduced the production of proinflammatory cytokines in HPDLCs stimulated with P gingivalis and its LPS.

CONCLUSION

The results suggested that TRAF6 may be a key molecule to control proinflammatory cytokine production induced by P gingivalis and its LPS. TRAF6 suppression may inhibit inflammatory responses in HPDLCs infected by P gingivalis and its LPS.