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Interleukin 1 gene expression in cultured human keratinocytes is augmented by ultraviolet irradiation.

机译:紫外线照射可增强培养的人角质形成细胞中白介素1基因的表达。

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摘要

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 cultured 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.
机译:白介素1(IL-1)是一类多肽,最初发现是由活化的单核细胞和巨噬细胞产生的,它们介导了多种对损伤和感染的细胞应答。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,最近已被证明与IL-1相同。人的表皮通常暴露于大量的太阳紫外线辐射下。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部分直接和长期病理后果的原因。在这项研究中,我们询问暴露于UVB辐射是否能在培养的人角质形成细胞中诱导IL-1基因表达。在没有明显刺激的情况下,培养的人角质形成细胞含有可检测量的IL-1α和βmRNA和蛋白质。暴露于10 ng / ml的12-O-十四烷酰-phorbol-13-乙酸盐(TPA)后6小时,这些水平可以显着提高。暴露于具有与日光相当的发射光谱的UVB辐射(与未过滤的人造UV光源相反),可显着提高相同人类角质形成细胞种群的稳态水平IL-1α和βmRNA。这些反映出这些培养物在体外产生的IL-1活性增加。在同一细胞群中,暴露于UVB辐射不会改变肌动蛋白mRNA的水平。因此,紫外线照射对IL-1的影响代表IL-1基因表达的特定增强。 IL-1的局部升高可能会介导急性UVB损伤的皮肤的炎症和血管舒张特征,而这种表皮IL-1的全身释放可能是发烧,白细胞增多以及过度日晒后出现的急性期反应。

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