Time-course evaluation and treatment of skin inflammatory immune response after ultraviolet B irradiation

• Published in: Cytokine (Philadelphia, Pa.) Pa.), 2008-10, Vol.44 (1), p.70-77
• Main Authors: Paz, Mariela L., Ferrari, Alejandro, Weill, Federico S., Leoni, Juliana, Maglio, Daniel H.Gonzalez
• Format: Article
• Language: English
• Subjects: Animals; Anti-Inflammatory Agents, Non-Steroidal - therapeutic use; Cell Line; Dermatitis - drug therapy; Dermatitis - etiology; Dermatitis - pathology; Dinoprostone - biosynthesis; Epidermis - pathology; Epidermis - radiation effects; Female; Humans; Immunity - radiation effects; Interleukin-6 - biosynthesis; Keratinocytes - radiation effects; Male; Mice; Naproxen - therapeutic use; Nitric Oxide Synthase Type II - biosynthesis; NSAID treatment; PGE 2; Skin - immunology; Skin - radiation effects; Skin inflammation; Time Factors; TNF-α; Tumor Necrosis Factor-alpha - biosynthesis; Ultraviolet Rays - adverse effects; UVB
• ISSN: 1043-4666; 1096-0023
• DOI: 10.1016/j.cyto.2008.06.012

Skin exposure to high doses of ultraviolet B (UVB) radiation generates a severe inflammatory skin response. In the present study we aim to investigate, using in vitro and in vivo models, the time-course of the inflammatory skin immune response after an acute exposure to UVB irradiation, as well as its modulation by a topical non-steroidal anti-inflammatory drug (NSAID) treatment, naproxen. PGE 2 production and TNF-α levels increase in a post-irradiation time-dependent manner both in vivo and in vitro. This production pattern is also reflected in the iNOS expression levels in vivo and in the IL-6 levels in vitro. Changes observed in these mediators are correlated with histological alterations and dermal infiltration after the acute UVB irradiation. Naproxen treatment notably reduces PGE 2 production and iNOS expression, reflecting the COX–NOS crosstalk already reported, although it causes an important increment in TNF-α synthesis in the epidermis of irradiated mice. Taken together, our data indicates that the epidermis is severely damaged by UVB radiation but then it is able to fully recover, and that the immune response is modulated by the NSAID treatment, since it is able to reduce the levels of some mediators as well as it can increase others.