Background: Molecular markers are involved in atopic dermatitis (AD) pathogenesis. The estrogen receptor (ESR)-1 gene, encoding ERα, is reported to express aberrantly in AD patients.
Objective: To detect the biological functions of ESR1 in 2,4 dinitrochlorobenzene (DNCB)-treated mice.
Methods: The DNCB-treated mice received a topical application of emulsion containing the 1,3-bis(4 hydroxyphenyl)-4-methyl-5-[4-(2-piperidinyl ethoxy) phenol]-1H-pyrazole dihydrochloride (MPP; an ESR1-selective antagonist) to dorsal skins and ears. Then the dermatitis scores, histopathological changes, and cytokine levels were evaluated.
Results: MPP specifically downregulated ESR1 expression in DNCB-applied mice. Functionally, application of MPP abolished the DNCB-induced promotion in dermatitis score. Additionally, MPP administration protected against DNCB-induced dermatitis severity, suppressed mast cell infiltration and reduced production of immunoglobulin E (IgE) and thymus and activation-regulated chemokine (TARC). Moreover, MPP treatment inhibited DNCB-induced production of Th2 cytokines and infiltration of CD4+ T cells.
Conclusion: ESR1 facilitates Th2-immune response and enhances Th2 cytokines in AD mice.
Keywords: Antagonist; Atopic Dermatitis; ESR1; Inflammatory Cytokines; Mice.