Abstract

Atopic dermatitis (AD) and psoriasis are the most common chronic inflammatory dermatitis treated with topical glucocorticoids (GC). Although long-term use of topical GC may induce skin atrophy including striae distensa (SD), AD patients appear to cause less skin atrophy compared to psoriasis. Chronic AD lesions are characterized by eosinophil infiltration and dermal fibrosis. Periostin, encoded by POSTN gene, augments TGF-β production in eosinophils and inversely activated eosinophils can induce periostin production in fibroblasts. Periostin involves in tissue remodeling such as fibrosis and lichenification of chronic AD lesion. This study was designed to reveal that AD patients have less skin atrophy due to skin fibrosis related with eosinophils and periostin compared to psoriasis. For the skin atrophy including SD, we enrolled AD and psoriasis patients with similar ages and treatment durations. For the skin fibrosis and eosinophils, we compared lesional and non-lesional skin from the patients with AD, psoriasis, and allergic contact dermatitis (ACD). Also, we compared mRNA expression in the dermis from the mouse model of AD or psoriasis. AD patients have less SD than psoriasis. In AD patients, the ratio of the dermal fibrous tissues was significantly higher than psoriasis. Tissue and blood eosinophils were significantly higher in AD patients than ACD as well as psoriasis. Dermal thickness and fibrosis were significantly higher in AD mice than psoriasis even after the treatment with topical GC. There was a significant positive correlation between dermal fibrosis and tissue eosinophils counts. The mRNAs of POSTN, TGFB1, COL11A1, MMP1, and IL1R2 were significantly up-regulated in AD mice than psoriasis. We found that AD patients had less skin atrophy than psoriasis after the long-term use of topical GC. It might be resulted from the skin fibrosis caused by upregulation of tissue eosinophils and periostin.

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