Enterococcus faecalis is a frequently isolated microorganism in persistent periapical lesion or secondary infection. However, no evidence has demonstrated that E. faecalis induced inflammation directly in the apical area. This study aimed to explore the mechanism of the inflammatory responses of human periodontal ligament fibroblasts (PDLs) to E. faecalis.Methods:
PDLs were stimulated with heat-killed E. faecalis (HKEF) or lipoteichoic acid from E. faecalis (LTA) with or without silencing of tumor necrosis factor receptor-associated factor 6 (TRAF6). The expressions of toll-like receptor 2/4, nucleotide-binding oligomerization domain 1/2, and TRAF6 were detected by using quantitative real-time polymerase chain reaction and Western blot. The secretions of proinflammatory cytokines, including interleukin-1β, interleukin-6, interleukin-8, and tumor necrosis factor-α, were determined in the cell supernatants with enzyme-linked immunosorbent assay.Results:
Both HKEF and LTA stimulated the expression of toll-like receptor 2 and TRAF6 in a time-dependent manner. The secretions of proinflammatory cytokines were also increased. After silencing TRAF6, the upregulations of proinflammatory cytokines induced by HKEF or LTA were attenuated.Conclusions:
TRAF6 plays a pivotal role in inflammation induced by E. faecalis or its LTA in PDLs.