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Induction of Proinflammatory Cytokines in Human Epidermoid Carcinoma Cells by in vitro Ultraviolet A1 Irradiation
Author(s) -
Morita Akimichi,
Grewe Markus,
GretherBeck Susanne,
OlaizolaHorn Sylvia,
Krutmann Jean
Publication year - 1997
Publication title -
photochemistry and photobiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.818
H-Index - 131
eISSN - 1751-1097
pISSN - 0031-8655
DOI - 10.1111/j.1751-1097.1997.tb01904.x
Subject(s) - tumor necrosis factor alpha , proinflammatory cytokine , cytokine , epidermoid carcinoma , microbiology and biotechnology , biology , cell culture , in vitro , downregulation and upregulation , cancer research , immunology , inflammation , biochemistry , carcinoma , gene , genetics
— Ultraviolet radiation‐induced expression of cytokines by keratinocytes is important for the pathogenesis of polymorphous light eruption (PLE). Because UVA1 radiation rather than UVB radiation might be a more important trigger for PLE, cells from the human epidermoid carcinoma cell line KB were exposed in vitro to UVA1 radiation (30 J/cm 2 ) and subsequently analyzed for cytokine expression. Ultraviolet A1 irradiation induced tumor necrosis factor (TNF)‐a and interleukin (IL)‐8 expression in KB cells at the mRNA and protein level. Upregulation of cytokine mRNA levels followed a Diphasic pattern. This effect was specific for TNFa and IL‐8 because UVA1 radiation did not induce expression of IL‐la or IL‐6 in these cells. Ultraviolet Al radiation‐induced expression of intercellular adhesion molecule‐1 in KB cells previously was found to depend on the thiol status of these cells. Therefore, KB cells were treated with DL‐buthionine‐[S, R]‐sulfoximine (BSO), a specific inhibitor of de novo glutathione synthesis. Exposure of BSO‐pretreated KB cells to UVA1 radiation significantly induced IL‐1α and IL‐6 mRNA and protein expression. These studies demonstrate the capacity of UVA1 radiation to induce cytokine expression in human epidermoid carcinoma cells. This immunomodulatory effect may be mediated by thiol‐status‐dependent and ‐independent mechanisms.