Lipopolysaccharide and cytokines induce nitric oxide synthase and produce nitric oxide in cultured normal human melanocytes.

The role of nitric oxide in normal and pathological conditions of human skin is still poorly understood. In this study we have demonstrated by immunobloting the expression of an inducible nitric oxide synthase isoform (iNOS) in cultured normal human melanocytes treated with bacterial lipopolysaccharide, tumor necrosis factor-alpha and interferon-gamma. Nitric oxide was also detected in the culture medium and its formation was abolished upon treatment with N(G)-mono-methyl-L-arginine(L-NMMA), a competitive inhibitor of nitric oxide synthase. These results suggest that nitric oxide could led to autodestruction of melanocytes causing skin depigmentation. The therapeutic relevance of nitric oxide synthase inhibitors in treatment of vitiligo was suggested.

Recognition of melanoma cell antigens with antibodies present in sera from patients with vitiligo.

BACKGROUND: Patients with vitiligo show specific losses of integumentary melanocytes, probably due to autoimmunity against melanocytes. We attempted to determine the presence of antibodies against pigment cell antigens in the sera of vitiligo patients. METHODS: Detergent-solubilized human melanoma cells were submitted to electrophoretic separation and immunoblotted against serum samples obtained from 19 patients with vitiligo and from 20 age- and sex-matched healthy individuals. RESULTS: Eighty-nine per cent of patients with vitiligo had antibodies to one or more pigment cell antigens. Similar antibodies were detected in 20% of healthy individuals. Antigens of 165, 90, and 68 kDa were recognized by the antibodies present in sera from 11%, 26%, and 37% of vitiligo patients, respectively, and in none of the normal sera. All patients with familial vitiligo also had antibodies to these three proteins. CONCLUSIONS: Proteins of 165, 90, and 68 kDa are specifically recognized by antibodies present in the sera of vitiligo patients and in all patients with genetic vitiligo. Whether or not these proteins might be implicated in the destruction of melanocytes by the immune system in vitiligo remains to be evaluated.