Lipoteichoic acid induces IL-6 production in human pulp stromal cells through TLR2-mediated NF-κB nuclear translocation

Objective This study aimed to investigate the inhibition of Toll-like receptor 2 (TLR2) signaling in lipoteichoic acid-induced NF-κB activation and interleukin-6 (IL-6) production in primary human dental pulp stromal cells (DPSCs). Design Primary human DPSCs were cultured with lipoteichoic acid from Staphylococcus aureus (LTA-SA; 10, 25, 50 µg/ml) for up to 72 h to assess time- and concentration-dependent IL-6 production. IL-6 secretion was quantified by ELISA, while cell counts were determined via cell counter. To evaluate TLR2-dependent signaling, cells were pre-incubated with the TLR2 inhibitor C29 (100 µM) prior to LTA-SA stimulation. IL6 gene expression was analyzed by RT-qPCR, and NF-κB nuclear translocation was assessed by Western blot analysis. Non-parametric statistical analyses were applied to compare all groups and time points (Mann-Whitney U test or Kruskal-Wallis test; α = 0.05). Results LTA-SA stimulation induced a significant, time- and concentration-dependent increase in IL6 gene expression and IL-6 secretion, accompanied by enhanced NF-κB nuclear translocation. Inhibition of TLR2 with C29 reduced nuclear translocation of NF-κB, along with a decrease in IL6 gene expression and IL-6 secretion, exhibiting both time- and concentration-dependent effects. Conclusions LTA induces IL-6 production in DPSCs via TLR2-mediated activation of the canonical NF-κB pathway. Targeted modulation of TLR2 signaling may represent a potential strategy for controlling pulpal inflammation.