P32Dexamethasone inhibits dendritic cell activation by skin sensitizers

Objective:  Evaluate activity of a corticosteroid on dendritic cell (DC) activation induced by skin sensitizers.
Methods:  Using a fetal mouse skin derived dendritic cell line (FSDC) stimulated by Nickel sulphate (50–100 ìg/ml) and DNFB (1–2.5 ìg/ml), we studied the effect of dexamethasone (DEX)(0.01–1 ìM) on nitric oxide (NO) production (by the Griess reaction), on nitric oxide synthase type II expression (iNOS)(by immunocytochemistry and western blot) and on the activation of the nuclear factor‐kappaB pathway (NF‐êB)(by electrophoretic mobility shift assay – EMSA), pathways that we have previously shown to be activated by these sensitizers.
Results:  NO production induced by Ni was significantly inhibited by DEX in a dose dependent way. Future studies using 0.5 ìM of DEX, showed a significant reduction of iNOS expression at 24 h induced by both sensitizers. This effect occurred in parallel with the inhibition of NF‐êB activation, which was most evident at 45 min.
Conclusions:  These results suggest that dexamethasone inhibits intracellular events that are relevant for DC activation induced by skin sensitizers during antigen presentation. Therefore, besides the anti‐inflammatory activity of DEX usually used for the treatment of ACD, this drug can also interfere with the initial steps of skin sensitization. This work was supported by FCT (Portugal).