抄録
Keratinocytes (KC) produce proinflammatory cytokines and prostaglandin E2 (PGE2) leading to the skin inflammation induced by ultraviolet radiation (UVR) . UVR-induced inflammation, sunburn, is mainly induced by UVB, but UVA is known to augment its reaction. In order to find if this augmentative effect of UVA is due to the effect of UVA on KC to induce proinflammatory mediators including cyto-kines and PGE2, normal human KC were cultured and irradiated by UVB and UVA either separately or concomitantly. Levels of mRNA for each cytokine were deter-mined by the reverse transcriptase-polymerase chain reaction (RT-PCR) method and protein production in cultured supernatants was assayed by enzyme-linked im-munosorbent assay (ELISA) or enzyme immunoassay (EIA) . UVB (300 J/m2) induced the expression of IL-6, IL-8, TNF-α, TGF-β1 and GM-CSF mRNA at 24 h after irradiation, while an increase only in IL-6 and IL-8 mRNA levels was observed at 24 h after UVA irradiation (10 kJ/m2) . IL-1α, IL 6, IL-8 and PGE2 production was increased augmentatively by UVB and UVA, but significant levels of TNF-α, TGF-β1 and GM-CSF protein in cultured supernatants were detected only after UVB irradiation. These results indicate that UVB and UVA differentially regulate the expression and production of KC-derived cytokines and UVA is able to induce proinflammatory mediators from KC additively to UVB. Our results explain the mechanism by which UVA augments UVB-induced skin inflammation.
