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紫外线B照射增强白细胞介素(IL)-6的产生及mRNA表达是由白细胞介素-1α在培养的人角质形成细胞中介导的。

Ultraviolet B irradiation-enhanced interleukin (IL)-6 production and mRNA expression are mediated by IL-1 alpha in cultured human keratinocytes.

作者信息

Chung J H, Youn S H, Koh W S, Eun H C, Cho K H, Park K C, Youn J I

机构信息

Department of Dermatology, Seoul National University College of Medicine, Korea.

出版信息

J Invest Dermatol. 1996 Apr;106(4):715-20. doi: 10.1111/1523-1747.ep12345608.

DOI:10.1111/1523-1747.ep12345608
PMID:8618010
Abstract

Ultraviolet (UV) B radiation may trigger cutaneous inflammatory responses by directly inducing epidermal keratinocytes to elaborate specific cytokines such as interleukin (IL-1) and IL-6. Because IL-1 is a potent inducer of IL-6, one may speculate that the release of IL-6 by keratinocytes after UV exposure is mediated via the release of IL-1 in an autocrine or paracrine manner. We demonstrated that UVB irradiation upregulated IL-1 alpha mRNA at a lower dose (15 mJ/cm2) and then downregulated IL-1 alpha mRNA expression at high doses (30-40 mJ/cm2). The kinetic profile of IL-1alpha mRNA expression showed a biphasic response, with the early increase by 1 h after UV exposure and the secondary increase at 6 h after UV. On the other hand, the expression of IL-6 mRNA was increased with increasing doses of UVB (0-45 m/J/cm2) and showed a single peak at 6 h post UV. These results may indicate that UVB radiation could regulate the expression of IL-1alpha and IL-6 mRNA in keratinocytes by different mechanisms. Our data show that anti-human IL-1alpha antibody inhibits UV-induced IL-6 production and mRNA expression in cultured keratinocytes. The addition of recombinant IL-1alpha to the medium increased IL-6 synthesis and augmented IL-6 production and mRNA expression in cultured human keratinocytes by UVB irradiation. These results support the hypothesis that UVB irradiation-enhanced IL-6 production and mRNA expression may be mediated by IL-1alpha.

摘要

紫外线B辐射可通过直接诱导表皮角质形成细胞产生特定细胞因子(如白细胞介素-1(IL-1)和IL-6)来引发皮肤炎症反应。由于IL-1是IL-6的强效诱导剂,因此有人推测紫外线照射后角质形成细胞释放IL-6是通过自分泌或旁分泌方式释放IL-1介导的。我们发现,低剂量(15 mJ/cm2)紫外线B照射可上调IL-1α mRNA表达,而高剂量(30 - 40 mJ/cm2)照射则下调IL-1α mRNA表达。IL-1α mRNA表达的动力学曲线呈现双相反应,紫外线照射后1小时出现早期增加,紫外线照射后6小时出现二次增加。另一方面,IL-6 mRNA表达随紫外线B剂量增加(0 - 45 mJ/cm2)而升高,并在紫外线照射后6小时出现单峰。这些结果可能表明紫外线B辐射可通过不同机制调节角质形成细胞中IL-1α和IL-6 mRNA的表达。我们的数据表明,抗人IL-1α抗体可抑制紫外线诱导的培养角质形成细胞中IL-6的产生和mRNA表达。向培养基中添加重组IL-1α可增加IL-6合成,并增强紫外线B照射后培养的人角质形成细胞中IL-6的产生和mRNA表达。这些结果支持以下假说:紫外线B照射增强的IL-6产生和mRNA表达可能由IL-1α介导。

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Ultraviolet B irradiation-enhanced interleukin (IL)-6 production and mRNA expression are mediated by IL-1 alpha in cultured human keratinocytes.紫外线B照射增强白细胞介素(IL)-6的产生及mRNA表达是由白细胞介素-1α在培养的人角质形成细胞中介导的。
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