Ultraviolet B radiation downregulates inducible nitric oxide synthase expression induced by interferon-gamma or tumor necrosis factor-alpha in murine keratinocyte Pam 212 cells.

Ultraviolet radiation causes inflammation characterized by erythema and swelling, but also exhibits antiinflammatory effects which have led to the use of ultraviolet B radiation (UVBR) and psoralen plus ultraviolet A (PUVA) in the treatment of psoriasis, chronic severe atopic dermatitis and uremic pruritus. In inflammatory dermatoses, a pathogenic role of nitric oxide (NO) derived from inducible nitric oxide synthase (iNOS) has been suggested. To elucidate how UVBR regulates iNOS expression in skin under inflammatory conditions, we investigated the effect of UVBR on NO production and iNOS expression in cultured murine keratinocyte Pam 212 cells stimulated with interferon-gamma (IFN-gamma) or tumor necrosis factor-alpha (TNF-alpha). Low doses of UVBR significantly suppressed IFN-gamma- or TNF-alpha-induced NO production. UVBR also downregulated IFN-gamma- or TNF-alpha-induced iNOS expression at both the mRNA level and the protein level. These findings suggest the possibility that the down-regulatory effect of UVBR on IFN-gamma- or TNF-alpha-induced iNOS expression may, in part, explain the antiinflammatory and therapeutic properties of UVBR in inflammatory dermatoses.