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首页> 外文期刊>Journal of dermatological science >Psoralen-ultraviolet A therapy alters epidermal Sema3A and NGF levels and modulates epidermal innervation in atopic dermatitis.
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Psoralen-ultraviolet A therapy alters epidermal Sema3A and NGF levels and modulates epidermal innervation in atopic dermatitis.

机译：补骨脂素-紫外线疗法可改变表皮Sema3A和NGF水平，并调节特应性皮炎中的表皮神经支配。

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BACKGROUND: Epidermal nerve densities are increased in patients with atopic dermatitis (AD), suggesting that it is partly responsible for the intense itching in the skin. Epidermal hyperinnervation in AD patients is decreased by ultraviolet (UV) phototherapy, although the underlying mechanisms are poorly understood. Interestingly, abnormal expression of axonal guidance molecules, such as nerve growth factor (NGF) and semaphorin 3A (Sema3A), is found in the epidermis of AD patients. Therefore, UV phototherapy may alter levels of axonal guidance molecule expression in atopic skin. OBJECTIVE: This study was performed to investigate whether epidermal Sema3A and NGF levels in AD are influenced by psoralen-UVA (PUVA) therapy. METHODS: Skin biopsies obtained from chronic AD patients before and after PUVA therapy were used. Both Sema3A and NGF in the skin were examined at mRNA and protein levels by quantitative RT-PCR and immunohistochemistry, respectively. Nerve fibers in the skin were stained with anti-PGP9.5 antibody, and the number of epidermal nerve fibers was counted. RESULTS: PUVA therapy decreased epidermal nerve densities in AD patients, concomitant with decreases in both visual analog scale (VAS) scores for pruritus and clinical severity scores. Increased fluorescence intensity of Sema3A and decreased fluorescence intensity of NGF were observed in the epidermis of PUVA-treated group. Moreover, Sema3A mRNA levels were upregulated in the PUVA-treated skins compared with untreated controls, while NGF mRNA levels in the skin were downregulated by the treatment. CONCLUSION: PUVA therapy may reduce epidermal hyperinnervation of AD by normalization of abnormal Sema3A and NGF expression in the epidermis.
机译：背景：特应性皮炎（AD）患者的表皮神经密度增加，这提示其部分引起皮肤强烈的瘙痒。紫外线（UV）光疗可减少AD患者的表皮过度神经支配，尽管其基本机制尚不清楚。有趣的是，在AD患者的表皮中发现了轴突引导分子，例如神经生长因子（NGF）和信号量3A（Sema3A）的异常表达。因此，紫外线光疗可能会改变特应性皮肤中轴突引导分子的表达水平。目的：本研究旨在研究补骨脂素-UVA（PUVA）治疗是否会影响AD中的表皮Sema3A和NGF水平。方法：使用从PUVA治疗前后的慢性AD患者获得的皮肤活检样本。分别通过定量RT-PCR和免疫组织化学检查了皮肤中Sema3A和NGF的mRNA和蛋白水平。用抗PGP9.5抗体将皮肤中的神经纤维染色，并计数表皮神经纤维的数量。结果：PUVA治疗降低了AD患者的表皮神经密度，同时伴有瘙痒症的视觉模拟量表（VAS）评分和临床严重程度评分的降低。在PUVA处理组的表皮中观察到Sema3A的荧光强度增加和NGF的荧光强度降低。此外，与未处理的对照组相比，PUVA处理的皮肤中Sema3A mRNA的水平上调，而皮肤中的NGF mRNA的水平则被该处理下调。结论：PUVA疗法可通过使表皮中异常的Sema3A和NGF表达正常化来减轻AD的表皮过度神经支配。

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