Ultraviolet B irradiation selectively increases the production of interleukin-8 in human cord blood-derived mast cells

UVB irradiation modulates immune responses in the skin and is a major cause of sunburn, during which neutrophils accumulate in the skin. Because of their abundance in skin and ability to produce a variety of proinflammatory mediators, we propose that mast cells may play a key role in ultraviolet B (...

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Bibliographic Details
Published in:Clinical and experimental immunology Vol. 148; no. 1; pp. 161 - 167
Main Authors: Endoh, I, Di Girolamo, N, Hampartzoumian, T, Cameron, B, Geczy, C.L, Tedla, N
Format: Journal Article
Language:English
Published: Oxford, UK Oxford, UK : Blackwell Publishing Ltd 01-04-2007
Blackwell Publishing Ltd
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Summary:UVB irradiation modulates immune responses in the skin and is a major cause of sunburn, during which neutrophils accumulate in the skin. Because of their abundance in skin and ability to produce a variety of proinflammatory mediators, we propose that mast cells may play a key role in ultraviolet B (UVB)-induced skin inflammation. Cord blood-derived human mast cells were treated in vitro with varying doses of UVB and production of multiple cytokines was measured in culture supernatants. UVB exposure significantly increased the release of interleukin (IL)-8 and modestly increased IL-1α production, but cytokines such as IL-2, IL-4, IL-6, IL-10, IL-12, IL-13, tumour necrosis factor (TNF)-α and interferon (IFN)-γ were unaffected. Cycloheximide reduced the UVB-mediated induction of IL-8 by 30-40%, suggesting that new protein synthesis contributed to IL-8 production. In line with this, UVB treatment of mast cells significantly increased IL-8 mRNA. In contrast to its effect on IL-8 production, optimal doses of UVB did not provoke histamine or tryptase release, indicating little effect on degranulation. Our data suggest that mast cells may play a major role during UVB-induced acute inflammation by selectively inducing cytokines involved in neutrophil recruitment.
Bibliography:http://dx.doi.org/10.1111/j.1365-2249.2007.03332.x
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ISSN:0009-9104
1365-2249
DOI:10.1111/j.1365-2249.2007.03332.x