Influence of TEGDMA on Surface Antigen Expression of Macrophages

Objective: Dental resin monomers like triethyleneglycoldimethacrylate (TEGDMA) caused cytotoxicity in a variety of cells. Here, we analysed the influence of TEGDMA on surface antigen expression of murine macrophages, that are a major component of the innate immune system.

Methods: RAW264.7 macrophages were exposed to 0.0–8.0 mM TEGDMA in culture medium for 6, 24 and 48h in the presence and absence of LPS (lipopolysaccharide). LPS from E.coli (25µg/ml) served as a positive control, and culture medium was the negative control. Cytotoxicity of LPS/TEGDMA was detected by crystal violet assay. The expression of the surface antigens CD40 (T-cell interaction), CD80/86 (costimulation), CD14 (LPS-binding), CD54 (cell adhesion), MHC I, and MHC II was determined by flow cytometry (FACS). Expression values were statistically examined by regression analyses and non-parametric procedures.

Results: The exposure of cells to TEGDMA alone did not change antigen expression, but stimulation with LPS/TEGDMA caused a concentration-dependent modification after a 24h period. Compared to the stimulation with LPS only, a combination of LPS/0.125mM TEGDMA resulted in a 27% decrease of CD40 expression, whereas 2mM TEGDMA induced a 98% reduction. CD80/CD86 expression was reduced by 9 and 13% with 0.125mM TEGDMA, and by 74 and 40% with 2mM, respectively. Contrary, low TEGDMA concentrations (0.125-0.25mM) increased CD14 expression by 9 and 27%, but higher concentrations (0.5-2.0mM) again decreased expression levels. LPS/2mM TEGDMA dropped the expression to 38% compared to LPS-induced effects. CD54 expression was increased by LPS/TEGDMA in a concentration-dependent manner by at least 1.8-fold. MHC I/MHC II expression was unremarkably affected by LPS and TEGDMA. The patterns of antigen expression were similar after a 48h exposure period, but only minor changes were detected after 6h. Decreased antigen expression was caused only in part by cell death.

Conclusion: These data indicate that TEGDMA interferes with the stimulatory potential of innate immune cells.