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Induction of interleukin-6 production by ultraviolet radiation in normal human epidermal keratinocytes and in a human keratinocyte cell line is mediated by DNA damage

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Author: Petit-Frère, C. · Clingen, P.H. · Grewe, M. · Krutmann, J. · Roza, L. · Arlett, C.F. · Green, M.H.L.
Type:article
Date:1998
Institution: Centraal Instituut voor Voedingsonderzoek TNO
Source:Journal of Investigative Dermatology, 3, 111, 354-359
Identifier: 234605
Keywords: Nutrition · (6-4) photoproduct · Cyclobutane pyrimidine dimers · DNA damage · Interleukin- 6 · Keratinocytes · Ultraviolet radiation · Cyclobutane · Deoxyribodipyrimidine photolyase · Dimer · Dna · Interleukin 6 · Liposome · Cancer cell culture · Dna damage · Human · Human cell · Keratinocyte · Priority journal · Sunburn · Ultraviolet b radiation · Ultraviolet c radiation · Ultraviolet radiation · Carcinoma, Squamous Cell · Cell Line · DNA Damage · Humans · Interleukin-6 · Keratinocytes · Pyrimidine Dimers · Reference Values · Ultraviolet Rays

Abstract

The sunburn reaction is the most common consequence of human exposure to ultraviolet radiation (UVR), and is mediated at least in part by interleukin- 6 (IL-6). The aim of this study was to determine if DNA is a major chromophore involved in the induction of IL-6 following UV irradiation of a human epidermoid carcinoma cell line (KB), and of normal human epidermal keratinocytes. We first confirmed that IL-6 release was associated with enhanced levels of IL-6 mRNA transcripts. The wavelength dependence for IL-6 release was then investigated by irradiating the cells at defined wavelengths (254, 302, 313, 334, and 365 nm) with a monochromator. The maximum effect on IL-6 release was observed at 254 nm with only low levels of induction observed at wavelengths above 313 nm. The wavelength dependence for UV- induced IL-6 release was similar to that for DNA absorption or for the induction of cyclobutane pyrimidine dimers (CPD). To determine whether UV- induced DNA damage mediated IL-6 secretion, the role of CPD was investigated by treating keratinocytes with photosomes (photolyase encapsulated in liposomes) followed by photoreactivating light. This photoreversal procedure led to a reduction in the levels of the UVC-induced secretion of IL-6, which in normal human keratinocytes was unambiguously associated with repair of CPD. We conclude that the release of IL-6 from human keratinocytes following short-wave UVC and UVB irradiation is mediated by DNA damage and that CPD play an important role in this process.