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特应性皮炎和浅表性皮肤损伤后抗菌肽的表达和分泌增强。

Enhanced expression and secretion of antimicrobial peptides in atopic dermatitis and after superficial skin injury.

机构信息

Department of Dermatology, Allergology, and Venerology, University Hospital Schleswig-Holstein, Campus Kiel, Kiel, Germany.

出版信息

J Invest Dermatol. 2010 May;130(5):1355-64. doi: 10.1038/jid.2009.432. Epub 2010 Jan 28.

DOI:10.1038/jid.2009.432
PMID:20107483
Abstract

Human skin can defend itself against potentially invading microorganisms by production of antimicrobial peptides (AMPs). The expression of AMPs in atopic dermatitis (AD) is still emerging. To gain more insight into the role of AMPs in AD, we systematically analyzed the expression of ribonuclease 7 (RNase 7), psoriasin, and human beta-defensins (hBD)-2 and -3 in AD compared with psoriatic and healthy control skin as well as after experimental barrier disruption. Immunostaining revealed enhanced expression of all AMPs in the lesional skin of untreated AD and psoriasis when compared with non-lesional skin and controls. Accordingly, induced in vivo secretion of RNase 7, psoriasin, and hBD-2 was detected using ELISA on lesional skin in AD and in even higher concentrations in psoriasis. The secretion of AMPs did not correlate with severity of AD and Staphylococcus aureus colonization. Skin barrier disruption caused enhanced immunoreactivity of hBD-2 and hBD-3 after 24 hours. Strong secretion of RNase 7 was already detected after 1 hour, whereas hBD-2 secretion was significantly enhanced after 24 hours only under occlusion. Thus, a disturbed skin barrier may trigger AMP induction in AD and psoriasis. The functional role of AMP in AD, especially with regard to the control of S. aureus colonization, needs further analysis.

摘要

人体皮肤可以通过产生抗菌肽(AMPs)来抵御潜在的入侵微生物。特应性皮炎(AD)中 AMP 的表达仍在不断出现。为了更深入地了解 AMP 在 AD 中的作用,我们系统地分析了 AD 与银屑病和健康对照组皮肤以及实验性屏障破坏后,核糖核酸酶 7(RNase 7)、角鲨烯和人β-防御素(hBD)-2 和 -3 的表达。免疫染色显示,与非病变皮肤和对照组相比,未经治疗的 AD 和银屑病病变皮肤中所有 AMP 的表达均增强。相应地,在 AD 的病变皮肤和甚至更高浓度的银屑病中,通过 ELISA 检测到体内诱导的 RNase 7、角鲨烯和 hBD-2 的分泌。AMP 的分泌与 AD 的严重程度和金黄色葡萄球菌定植无关。皮肤屏障破坏导致 24 小时后 hBD-2 和 hBD-3 的免疫反应性增强。1 小时后即可检测到 RNase 7 的强烈分泌,而仅在闭塞下 24 小时后 hBD-2 的分泌才显著增强。因此,皮肤屏障的破坏可能会引发 AD 和银屑病中 AMP 的诱导。AMP 在 AD 中的功能作用,特别是在控制金黄色葡萄球菌定植方面,需要进一步分析。

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