INTERLEUKIN-1 GENE-EXPRESSION IN CULTURED HUMAN KERATINOCYTES IS AUGMENTED BY ULTRAVIOLET-IRRADIATION
INTERLEUKIN-1 GENE-EXPRESSION IN CULTURED HUMAN KERATINOCYTES IS AUGMENTED BY ULTRAVIOLET-IRRADIATION
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DOI：
10.1172/jci113090
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发表时间：
1987-08-01
影响因子：
15.9
通讯作者：
GUBLER, U
中科院分区：
文献类型：
--
作者：
KUPPER, TS;CHUA, AO;GUBLER, U
白细胞介素1（IL-1）是最初发现由活化的单核细胞和巨噬细胞产生的多肽家族，其介导对损伤和感染的多种细胞应答。表皮上皮细胞（角质形成细胞）产生“表皮细胞衍生的胸腺细胞激活因子”或ETAF，最近已证明其与IL-1相同。人体表皮通常暴露于大量的太阳紫外线辐射。某些紫外线波长（UVB，290-320 nm）被认为是过度暴露于阳光下的大多数直接和长期病理后果的原因。在这项研究中，我们问是否暴露于UVB照射诱导白细胞介素-1基因在培养人角质形成细胞的表达。培养的人角质形成细胞含有可检测量的IL-1 α。和βmRNA和蛋白质在没有明显的刺激;这些水平可以显着增强6小时后，暴露于10 ng/ml的12-O-十四酰基-佛波醇-13-乙酸酯（TPA）。暴露于发射光谱与日光相当的UVB照射（与未过滤的人工UV光源的发射光谱相反）显著增加了IL-1 α的稳态水平。和β在相同的人角质形成细胞群体中的mRNA。这反映在这些培养物在体外产生增加的IL-1活性。在相同的细胞群体中，暴露于UVB照射并没有改变肌动蛋白mRNA的水平，因此，紫外线照射对IL-1的影响代表了IL-1基因表达的特异性增强。局部IL-1的增加可能介导急性UVB损伤皮肤的炎症和血管舒张特征，并且这种表皮IL-1的全身释放可能导致发热、白细胞增多和过度日光暴露后观察到的急性期反应。
Interleukin 1 (IL-1) is a family of polypeptides initially found to be produced by activated monocytes and macrophages that mediate a wide variety of cellular responses to injury and infection. Epidermal epithelial cells (keratinocytes) produce "epidermal cell-derived thymocyte activating factor" or ETAF, which has been recently shown to be identical to IL-1. Human epidermis is normally exposed to significant amounts of solar ultraviolet radiation. Certain ultraviolet wavelengths (UVB, 290-320 nm) are thought to be responsible for most of the immediate and long-term pathological consequences of excessive exposure to sunlight. In this study, we asked whether exposure to UVB irradiation induced IL-1 gene expression in culture human keratinocytes. Cultured human keratinocytes contain detectable amounts of IL-1 .alpha. and .beta. mRNA and protein in the absence of apparent stimulation; these levels could be significantly enhanced 6 h after exposure to 10 ng/ml of 12-O-tetradecanoyl-phorbol-13-acetate (TPA). Exposure to UVB irradiation with an emission spectrum comparable to that of sunlight (as opposed to that of an unfiltered artificial UV light source) significantly increased the steady state levels IL-1.alpha. and .beta. mRNA in identical populations of human keratinocytes. This was reflected in the production of increased IL-1 activity by these cultures in vitro. In the same cell population, exposures to UVB irradiation did not alter the level of actin mRNA; therefore, the effect of UV irradiation on IL-1 represents a specific enhancement of IL-1 gene expression. Local increases of IL-1 may mediate the inflammation and vasodilation characteristic of acute UVB-injured skin, and systemic release of this epidermal IL-1 may account for fever, leukocytosis, and the acute phase response seen after excessive sun exposure.