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紫外线A1和紫外线B照射对人皮肤中肿瘤坏死因子-α诱导的对比作用。

Contrasting effects of ultraviolet A1 and ultraviolet B exposure on the induction of tumour necrosis factor-alpha in human skin.

作者信息

Skov L, Hansen H, Allen M, Villadsen L, Norval M, Barker J N, Simon J, Baadsgaard O

机构信息

Department of Dermatology, Gentofte Hospital, University of Copenhagen, Hellerup, Denmark.

出版信息

Br J Dermatol. 1998 Feb;138(2):216-20. doi: 10.1046/j.1365-2133.1998.02063.x.

Abstract

Ultraviolet B (UVB) irradiation of the skin causes immunosuppression which is relevant to the induction of skin cancer. The mechanism of this immunomodulation is unclear but various regulatory molecules have been implicated, including cis-urocanic acid (cis-UCA) and the cytokines tumour necrosis factor-alpha (TNF-alpha) and interleukin 10 (IL-10). Whether ultraviolet A (UVA) induces similar changes has not been investigated fully. We studied the effect of in vivo UVB and long-wave UVA (UVA1) exposure on the induction of TNF-alpha, IL-10 and cis-UCA in human skin. Volunteers were irradiated with three minimal erythema doses (MED) of UVB or UVA1. At different times after irradiation, suction blisters were raised from irradiated and from non-irradiated (control) skin. The TNF-alpha and IL-10 protein concentration, and the percentage of cis-UCA in the blister fluid, were then determined. UVB irradiation of human skin led to a rapid and significant increase in TNF-alpha concentration in suction-blister fluid, with maximal values 6 h after irradiation (n = 6, P < 0.05). In contrast, UVA1 irradiation led to a decrease in TNF-alpha concentration in the suction-blister fluid compared with non-irradiated skin, with the lowest values 6 h after irradiation (n = 6, P < 0.05). Both UVB and UVA1 exposure of the skin induced a slight increase in IL-10 concentration. However, the increase in IL-10 was only significant after UVB irradiation (UVB, n = 6, P < 0.05; UVA, n = 7, P < 0.1). As previously shown, both UVB and UVA1 result in the photo-isomerization of trans-UCA and an increased percentage of cis-UCA was found in the suction-blister fluid. Thus the results show differential effects of UVB and UVA1 irradiation on the induction of immunoregulatory molecules, which may help to explain the variation in immune responses after UVB and UVA1 exposure of human skin.

摘要

皮肤的紫外线B(UVB)照射会导致免疫抑制,这与皮肤癌的诱发相关。这种免疫调节的机制尚不清楚,但多种调节分子被认为与之有关,包括顺式尿刊酸(cis-UCA)以及细胞因子肿瘤坏死因子-α(TNF-α)和白细胞介素10(IL-10)。紫外线A(UVA)是否会引发类似变化尚未得到充分研究。我们研究了体内UVB和长波UVA(UVA1)照射对人皮肤中TNF-α、IL-10和cis-UCA诱导的影响。志愿者接受了三次UVB或UVA1的最小红斑剂量(MED)照射。在照射后的不同时间,从照射部位和未照射(对照)皮肤处引出负压水疱。然后测定水疱液中TNF-α和IL-10的蛋白浓度以及cis-UCA的百分比。人皮肤的UVB照射导致负压水疱液中TNF-α浓度迅速且显著增加,照射后6小时达到最大值(n = 6,P < 0.05)。相比之下,与未照射皮肤相比,UVA1照射导致负压水疱液中TNF-α浓度降低,照射后6小时达到最低值(n = 6,P < 0.05)。皮肤暴露于UVB和UVA1均会导致IL-10浓度略有增加。然而,IL-10仅在UVB照射后显著增加(UVB,n = 6,P < 0.05;UVA,n = 7,P < 0.1)。如先前所示,UVB和UVA1均会导致反式UCA的光异构化,并且在负压水疱液中发现顺式UCA的百分比增加。因此,结果显示UVB和UVA1照射对免疫调节分子诱导的不同影响,这可能有助于解释人皮肤暴露于UVB和UVA1后免疫反应的差异。

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