Abstract

Sunburn is prevalent and while the clinical effects disappear quickly, repeated episodes have long term consequences such as skin cancer. Pro-inflammatory eicosanoid expression and leukocyte infiltration characterise the peak of the sunburn response, however, little is known of these processes during the resolution phase. We examined changes in eicosanoid expression and leukocyte infiltration up to 14 days post acute sunburn. Photoprotected buttock skin was exposed to 3xMED of broadband UVR and skin erythema measured over 14 days (n=13; 20-58yrs, 8F, phototype I-III). Biopsies and suction blister fluid were sampled from unexposed and UVR-exposed skin over the 14 day time-course and analysed by immunohistochemistry (neutrophil elastase, CD4, CD8, CD68, CD1a, COX-2, EP4) and LC-MS/MS (eicosanoids). Erythema, COX-2, eicosanoid production and infiltration of innate immune cells (neutrophils and macrophage), peaked at D1 post UVR. By D7 erythema showed 60% resolution, while expression of the prostaglandin E2 receptor EP4 remained elevated at D14. Infiltration of adaptive immune cells (CD4+, CD8+ T cells) peaked at D4-D7 and remained above baseline at D14 (p<0.01, p<0.001 respectively). Moreover, the CD4+:CD8+ ratio rose post-UVR, peaking at 4.3:1 at D1, compared with 2:1 at D0. In contrast, epidermal Langerhans cell numbers showed maximum reduction (∼50%) at D4-D7 (p<0.01), only fully returning to baseline at D14. Acute UVR exposure has profoundly impacts epidermal antigen presenting cell number persisting for up to 2 weeks following the initial insult. Thus a single sunburn may trigger a prolonged immunosuppressive environment compromising ability to respond to neoplastic change and exogeneous challenge.

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