Inhibitory effects of 2-hydroxyethyl methacrylate on IL-1β-induced NF-κB activation and chemokine production in human gingival fibroblasts.

2-Hydroxyethyl methacrylate (HEMA) is the most abundantly released monomer from dental restorative materials, and it has been suggested that it may also affect periodontal tissue cells. This study aimed to clarify the influence of HEMA on gingival inflammation, focusing particularly on its effects on chemokine production involved in leukocyte migration and on the signaling pathways regulating their expression in human gingival fibroblasts (HGFs). Chemokine production from interleukin (IL)-1β-stimulated HGFs was evaluated using an enzyme-linked immunosorbent assay (ELISA), and the phosphorylation of mitogen-activated protein kinases (MAPKs) and nuclear factor (NF)-κB, the nuclear translocation of NF-κB p65, and the expression of heme oxygenase-1 (HO-1) were examined by Western blot analysis. HEMA inhibited IL-1β-induced production of chemokines (CCL2, CCL20, CXCL10, and IL-8) in a concentration-dependent manner. Although HEMA did not affect the activation of MAPKs, it suppressed the activation of the NF-κB pathway and reduced the nuclear translocation of NF-κB p65 in IL-1β-stimulated HGFs. Furthermore, HEMA treatment increased HO-1 expression in HGFs. These findings suggest that HEMA may influence the immune response in periodontal lesions by suppressing chemokine production in HGFs.