DNA methylation is one of major epigenetic mechanisms by which regulate a panel of gene expressions. An old but a revisiting compound, 5-azacytidine, is a pyrimidine nucleoside analog of cytidine that can inhibit DNA methyltransferase, induce cell differentiation, and has direct cytotoxicity on abnormal bone marrow hematopoietic cells. Thus, systemic administration of 5-azacytidine has been approved for the treatment of myelodysplastic syndrome and acute myeloid leukemia. However, the effect of topical 5-azacytidine on skin inflammation is largely unknown. To this end, we utilized croton oil (CrO)-induced irritant contact dermatitis (ICD) model and 2,4-dinitrofluorobenzene (DNFB)-induced allergic contact dermatitis (ACD) model. At day -1, vehicle or 1 mg of 5-azacytidine solution was applied to each ear. At day 0, 1% CrO was applied to both ear, and ear thickness was measured over time. Interestingly, the ear swelling response to CrO in 5-azacytidine-treated ear was significantly increased and prolonged compared with that of vehicle-treated ear. In DNFB-induced ACD model, topical application of 1 mg of 5-azacytidine solution to the abdomen one day before the sensitization with 0.5% DNFB did not alter following ear swelling. In sharp contrast, topical application of 1 mg of 5-azacytidine solution to the ear of 0.5% DNFB-sensitized mice one day before the elicitation with 0.2% DNFB significantly decreased ear swelling compared with that of vehicle applied ear. These data suggest that topical 5-azacytidine differently influences ICD and ACD as well as sensitization phase and elicitation phase of ACD. Topical 5-azacytidine must modify a bunch of gene and protein expressions. However, it could be a therapeutic option of ACD.

ESDR060 - The effect of topical 5-azacytidine in irritant and allergic contact dermatitis

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