Ultraviolet B irradiation-enhanced interleukin (IL)-6 production and mRNA expression are mediated by IL-1 alpha in cultured human keratinocytes

Ultraviolet (UV) B radiation map trigger cutaneous inflammatory responses by directly inducing epidermal keratinocytes to elaborate specific cytokines such as interleukin (IL)-1 and IL-6. Because IL-1 is a potent inducer of IL-6, one may speculate that the release of IL-6 by keratinocytes after UV exposure is mediated via the release of IL-1 in an autocrine or paracrine manner. We demonstrated that UVB irradiation upregulated IL-1 alpha mRNA at a lower dose (15 mJ/cm(2)) and then downregulated IL-1 alpha mRNA expression at high doses (30-40 mJ/cm(2)). The kinetic profile of IL-1 alpha mRNA expression showed a biphasic response, with the early increase by 1 h after UV exposure and the secondary increase at 6 h after UV. On the other hand, the expression of IL-6 mRNA was increased with increasing doses of UVB (0-45 mJ/cm(2)) and showed a single peak at 6 h post-UV. These results may indicate that UVB radiation could regulate the expression of IL-1 alpha and IL-6 mRNA in keratinocytes by different mechanisms. Our data show that antihuman IL-1 alpha antibody inhibits UV-induced IL-6 production and mRNA expression in cultured keratinocytes. The addition of recombinant IL-1 alpha to the medium increased IL-6 synthesis and augmented IL-6 production and mRNA expression in cultured human keratinocytes by UVB irradiation, These results support the hypothesis that UVB irradiation-enhanced IL-6 production and mRNA expression may be mediated by IL-1 alpha.