Tumour necrosis factor‐α is involved in the contrasting effects of ultraviolet B and ultraviolet A1 radiation on the release by normal human keratinocytes of vascular permeability factor

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Abstract
Erythema and the initiation of an inflammatory response are typical features of human skin after ultraviolet (UV) radiation (UVR) exposure. Among the soluble factors that account for the induction of an erythema, the most recently discovered is vascular permeability factor/vascular endothelial growth factor (VPF/VEGF), a potent inducer of microvascular permeability which is expressed by keratinocytes. As epidermal cells are the first target cells of UVR, we studied the effects of UVBR (312 nm) and UVA1R (365 nm) on the secretion of VEGF by normal human keratinocytes and evaluated the role of interleukin 1α (IL-1α) and tumour necrosis factor-α (TNF-α) in this process. UVBR (100 and 200 mJ/cm2) induced a dose-dependent increase in the release by normal human keratinocytes of VEGF, which is widely mediated through the release of TNF-α but not IL-1α. Conversely, UVA1R (5 and 7 J/cm2) did not modify the basal level of VEGF and did not induce the secretion of TNF-α by keratinocytes. Moreover UVA1R, when associated with UVBR, inhibited the increase in VEGF induced by UVBR alone. Taken together, these findings indicate that UVBR and UVA1R have a contrasting effect on the release of VEGF, which is widely mediated by TNF-α. They may partly explain the minor erythematous effect of UVA1R and its beneficial role in cutaneous phototherapy.

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