Abstract
Abstract Histamine is an important inflammatory mediator in atopic dermatitis. The histamine H4 receptor (H4R), primarily expressed on immune cells, affects Th2 responses, dendritic cell functions, eosinophil and mast cell chemotaxis. Recent studies also demonstrate its role in experimental pruritus. In this study, we investigated the function of H4R in a Th2-dependent mouse model of atopic dermatitis. Mice were sensitized with Fluorescein isothiocyanate (FITC) on the abdominal skin, and later challenged with FITC on the ear. Ear edema and pruritic response were then evaluated. The experimental group that received JNJ7777120, a potent and specific H4R antagonist, developed less edema (28%, P <0.01) and pruritic response (68%, P <0.05). JNJ7777120 administration also inhibits cytokine and chemokine production measured from homogenates of inflamed ear. Taken together, these results suggest that the H4R is involved in inflammatory responses in this Th2-dependent atopic dermatitis model. Therefore, antagonists to the H4R may be an effective treatment for atopic dermatitis, given their dual anti-inflammatory and anti-pruritic effects.
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