ABSTRACT
BACKGROUND: Keratinocyte-derived interleukin-1(IL-1)alpha is one of the key cytokines in initiation of cutaneous inflammation. Release of IL-1alpha from human keratinocytes may be induced by proinflammatory stimuli including ultraviolet B(UVB) irradiation, and subsequently, keratinocyte-derived IL-1alpha may exert numerous paracrine and autocrine effects. 1,25-dihydroxyvitamin D3(1,25(OH)2D3) is involved in the regulation of keratinocyte proliferation and differentiation and is also recognized to have immunoregulatory properties such as an antiinflammatory effect. OBJECTIVE: The purpose of this study was to investigate the in vitro effects of 1,25-(OH)2D3 on the production of IL-1alpha by UVB irradiation in cultured human keratinocyte cell line HaCaT cells. RESULTS: are summerized as follows; 1. The vialility of cultured HaCaT cells measured by MTS assay at 24 hours after UVB irradiation was significantly reduced at the doses of above 100 mJ/cm2 of UVB(p<0.05). 2. The secretion of IL-1alpha by HaCaT cells was significantly increased at the doses of above 30 mJ/cm2 of UVB(p<0.05). UVB irradiation could not influence on the secretion of IL-1beta by HaCaT cells. 3. At the concentrations of 10-8M and 10-6M of 1,25(OH)2D3, the production of IL-1alpha by HaCaT cells(48 hours after 100 mJ/cm2 UVB irradiation) was significantly inhibited in both culture supernatants and cell lysates(p<0.05). CONCLUSION: UVB irradiation increased the production of IL-1alpha by HaCaT cells and this stimulatory effect on the production of IL-1alpha induced by UVB irradiation was suppressed by 1,25-(OH)2D3. Calcipotriol(MC-903) had similar suppressive effect on the production of IL-1alpha induced by UVB irradiation in HaCaT cells to that of 1,25(OH)2D3.