Loss of epidermal p38? signaling prevents UVR-induced inflammation via acute and chronic mechanisms.

ABSTRACT: UVB is a component of solar radiation primarily responsible for causing damage and cancer in irradiated skin, and disrupting immune homeostasis. The immediate harm and long-term health risks of excessive sunlight exposure are affecting the lives of nearly all people worldwide. Inflammation is a key mechanism underlying UVB's various detrimental effects. Here we show that activation of the protein kinase p38? is restricted to the epidermis in UVB-exposed skin, and that p38? ablation targeted to the epithelial compartment is sufficient to suppress UVB-induced inflammation. Mechanistically, loss of epithelial p38? signaling attenuates the expression of genes required to induce vascular leakage and edema, and also increases the steady-state abundance of epidermal ?? T cells, which are known to promote the repair of damaged epidermis. These effects of p38? deficiency delineate a molecular network operating at the organism-environment interface, and reveal conditions crucial to preventing the pathology resulting from sun-damaged skin.

SUBMITTER: Sano Y 

PROVIDER: S-EPMC4102657 | biostudies-literature | 2014 Aug

REPOSITORIES: biostudies-literature