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

Ultraviolet radiation causes inflammation characterized by erythema and swe lling, but also exhibits antiinflammatory effects which have led to the use of ultraviolet B radiation (UVBR) and psoralen plus ultraviolet A (PUVA) i n the treatment of psoriasis, chronic severe atopic dermatitis and uremic p ruritus. 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 co nditions, we investigated the effect of UVBR on NO production and iNOS expr ession in cultured murine keratinocyte Pam 512 cells stimulated with interf eron-gamma (IFN-gamma) or tumor necrosis factor-alpha (TNF-alpha). Low dose s of UVBR significantly suppressed IFN-gamma- or TNF-alpha-induced NO produ ction. UVBR also downregulated IFN-gamma- or TNF-alpha-induced iNOS express ion at both the mRNA level and the protein level. These findings suggest th e possibility that the down-regulatory effect of UVBR on IFN-gamma- or TNF- alpha-induced iNOS expression may, in part, explain the antiinflammatory an d therapeutic properties of UVBR in inflammatory dermatoses.