RESUMO
Ultraviolet ray B (UV-B) induced dermatitis in the rat may be a model for human psoriasis vulgaris. Detailed studies of this model are reported. Rat skin responded to UV-B irradiation quite differently from human, guinea-pig, or mouse skin. Rat UV-B dermatitis was characterized by a sharply demarcated brownish-red lesion with scale formation lasting for 10 days. Histologically, microvascular dilatation, intraepidermal accumulation of polymorphonuclear leucocytes with microabscess, mononuclear cell infiltration at the papillary dermis and hyperproliferation of epidermal cells were observed. These features were similar to those of clinical psoriasis vulgaris in man. Leucocyte suppression, induced by systemic ferritin administration to the irradiated rats, resulted in loss of the epidermal hyperproliferation and inhibition of the tissue leucocytosis. This leucocyte suppression remodelled the picture of the rat UV-B dermatitis into that seen in other mammalian species, where microvascular dilatation and degeneration of keratinocytes (so-called sunburn cells) are characteristic. The irradiated epidermis of the rats treated with ferritin possessed an in vitro PMN chemotactic property. Rat UV-B dermatitis seems to be a useful model to investigate aetiopathogenic mechanisms in psoriasis vulgaris. However, the former heals after injury and does not relapse as does psoriasis.
Assuntos
Modelos Animais de Doenças , Transtornos de Fotossensibilidade/patologia , Psoríase/patologia , Pele/patologia , Raios Ultravioleta , Animais , Divisão Celular/efeitos da radiação , Quimiotaxia de Leucócito/efeitos da radiação , Epiderme/patologia , Epiderme/efeitos da radiação , Ferritinas/farmacologia , Leucócitos/efeitos dos fármacos , Masculino , Neutrófilos/fisiologia , Transtornos de Fotossensibilidade/etiologia , Ratos , Ratos Endogâmicos , Ratos Wistar , Pele/efeitos da radiaçãoRESUMO
Leukotriene B4 in the skin was remarkably elevated in the rat, but not in the guinea pig or the mouse 48 h after UV-B irradiation. These results were consistent with interspecies difference of PMN infiltration caused by UV-B irradiation. LTB4 in the rat skin was determined by both high-performance liquid chromatography and radioimmunoassay. LTB4 in the rat skin started to increase 24 h after irradiation and became about 65-fold higher in the irradiated site than in the nonirradiated site at the end of 48 h. This elevation was strongly inhibited by topical application of two 5-lipoxygenase inhibitors, AA-861 and piriprost, although the inflammatory reaction or infiltration of polymorphonuclear leukocytes was not much improved.
