The role of interleukin‐17 in mouse models of atopic dermatitis and contact dermatitis

E-ISSN： 1365-2230|40|6|665-671

ISSN： 0307-6938

Source： CLINICAL & EXPERIMENTAL DERMATOLOGY, Vol.40, Iss.6, 2015-08, pp. : 665-671

Disclaimer: Any content in publications that violate the sovereignty, the constitution or regulations of the PRC is not accepted or approved by CNPIEC.

Previous Menu Next

Abstract

SummaryBackgroundAtopic dermatitis (AD) and contact dermatitis (CD) are both T cell‐mediated eczematous disorders. Interleukin (IL)‐17, expressed by T helper (Th)17 cells, is involved in recruitment of inflammatory cells into AD and CD skin.AimIn this study, we investigated whether IL‐17 regulates immune dysregulation and affects skin barrier in oxazolone (OXA)‐induced AD‐like and CD‐like disease models in mice, by comparing IL‐17 null mutant (IL‐17−/−) vs. wild‐type (WT) mouse strains in the models.MethodsIL‐17−/− and WT Balb/c mice were used for OXA induction of AD‐like and CD‐like skin diseases. Ear swelling was measured by a micrometer. Skin biopsies were obtained for RNA isolation and histology. Real‐time quantitative PCR analysis was performed to quantify mRNA expression of Th2 cytokines. Skin permeability was measured by a vapometer, and structural changes in the skin were evaluated by electron and confocal microscopy.ResultsBoth OXA‐induced AD and CD responses were alleviated in IL‐17−/− mice relative to WT, as demonstrated by reductions in ear swelling, inflammatory cell infiltration and levels of Th2 cytokines. These endpoints were used to characterize inflammatory dysregulation in both AD and CD models. Skin‐barrier dysfunction, measured by increases in transepidermal water loss and dysfunction of lamellar bodies, and reductions in lipid distribution, were seen in both AD and CD in WT mice. In IL‐17−/− mice, however, these responses were significantly diminished.ConclusionsThe results indicate that the IL‐17 gene may play a role in modulating immune dysregulation and affecting skin barrier in OXA‐induced AD‐like and CD‐like skin disease models in the Balb/c mouse.