Nakaguma H, Kambara T, Yamamoto T
Department of Neuroscience and Immunology, Kumamoto University Graduate School of Medical Sciences, Japan.
Int J Exp Pathol. 1995 Feb;76(1):65-73.
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.
紫外线B（UV-B）诱导的大鼠皮炎可能是寻常型人类银屑病的一种模型。本文报道了对该模型的详细研究。大鼠皮肤对UV-B照射的反应与人类、豚鼠或小鼠皮肤有很大不同。大鼠UV-B皮炎的特征是有界限分明的棕红色皮损，并伴有鳞屑形成，持续10天。组织学上，观察到微血管扩张、多形核白细胞在表皮内积聚并形成微脓肿、乳头真皮层有单核细胞浸润以及表皮细胞过度增殖。这些特征与人类临床寻常型银屑病相似。给受照射大鼠全身注射铁蛋白诱导白细胞抑制，导致表皮过度增殖消失并抑制组织白细胞增多。这种白细胞抑制使大鼠UV-B皮炎的表现转变为其他哺乳动物物种所见的情况，其特征是微血管扩张和角质形成细胞变性（所谓的晒伤细胞）。用铁蛋白处理的大鼠受照射表皮具有体外中性粒细胞趋化特性。大鼠UV-B皮炎似乎是研究寻常型银屑病发病机制的有用模型。然而，前者损伤后会愈合，不会像银屑病那样复发。
