Induction of proinflammatory cytokines in human epidermoid carcinoma cells by in vitro ultraviolet A1 irradiation.

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/cm2) and subsequently analyzed for cytokine expression. Ultraviolet A1 irradiation induced tumor necrosis factor (TNF)-alpha and interleukin (IL)-8 expression in KB cells at the mRNA and protein level. Upregulation of cytokine mRNA levels followed a biphasic pattern. This effect was specific for TNF alpha and IL-8 because UVA1 radiation did not induce expression of IL-1 alpha or IL-6 in these cells. Ultraviolet A1 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-1 alpha 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.