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葡萄球菌肠毒素A在特应性皮炎中的潜在免疫炎症作用:免疫组织病理学分析及体外试验

Potential Immunoinflammatory Role of Staphylococcal Enterotoxin A in Atopic Dermatitis: Immunohistopathological Analysis and in vitro Assay.

作者信息

Lee Hee-Woo, Kim Sung Min, Kim Jung Min, Oh Byung Min, Kim Jun Young, Jung Han Jin, Lim Hyun Jung, Kim Byung Soo, Lee Weon Ju, Lee Seok-Jong, Kim Do Won

机构信息

Department of Veterinary Internal Medicine, College of Veterinary Medicine, Seoul National University, Seoul, Korea.

出版信息

Ann Dermatol. 2013 May;25(2):173-80. doi: 10.5021/ad.2013.25.2.173. Epub 2013 May 10.

DOI:10.5021/ad.2013.25.2.173
PMID:23717008
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3662910/
Abstract

BACKGROUND

The underlying mechanism of atopic dermatitis (AD) exacerbated by Staphylococcus aureus has not been established. However, we demonstrated recently that the majority of S. aureus strains colonized in the skin of Korean AD patients carried genes encoding staphylococcal enterotoxin A (SEA) and/or toxic shock syndrome toxin-1 (TSST-1).

OBJECTIVE

To clarify the role of staphylococcal superantigen, SEA in AD.

METHODS

With the lesional skin of 9 AD patients and normal looking skin of one healthy adult, we examined first the expression of SEA, staphylococcal enterotoxin B (SEB), and TSST-1 using immunohistochemical analysis. In addition, we investigated the effects of SEA on the expression of inflammation-related adhesion molecules and cytokines in human HaCaT keratinocytes and Human Umbilical Vein Endothelial Cells (HUVECs) by reverse transcriptase-polymerase chain reaction (RT-PCR) analysis and enzyme-linked immunosorbent assay.

RESULTS

Staphylococcal protein A (SPA) and SEA were detected with increased immunoreactivity in AD patients. However, TSST-1 showed mild-to-moderate immunoreactivity in AD patients, whereas SEB was minimally detected. In the double immunofluorescence investigation, SEA and SPA were well co-localized. SEA induced upregulation of adhesion molecules and elicited inflammatory responses in HaCaT keratinocytes and HUVECs.

CONCLUSION

This study demonstrates the importance of SEA as an immunoinflammatory triggering factor of AD in Koreans.

摘要

背景

金黄色葡萄球菌加重特应性皮炎(AD)的潜在机制尚未明确。然而,我们最近证实,韩国AD患者皮肤中定植的大多数金黄色葡萄球菌菌株携带编码葡萄球菌肠毒素A(SEA)和/或中毒性休克综合征毒素-1(TSST-1)的基因。

目的

阐明葡萄球菌超抗原SEA在AD中的作用。

方法

我们选取9例AD患者的皮损及1名健康成年人外观正常的皮肤,首先采用免疫组化分析检测SEA、葡萄球菌肠毒素B(SEB)和TSST-1的表达。此外,我们通过逆转录聚合酶链反应(RT-PCR)分析和酶联免疫吸附测定,研究SEA对人HaCaT角质形成细胞和人脐静脉内皮细胞(HUVECs)中炎症相关黏附分子和细胞因子表达的影响。

结果

在AD患者中检测到葡萄球菌蛋白A(SPA)和SEA的免疫反应性增加。然而,TSST-1在AD患者中显示出轻度至中度的免疫反应性,而SEB检测到的量极少。在双重免疫荧光研究中,SEA和SPA共定位良好。SEA诱导HaCaT角质形成细胞和HUVECs中黏附分子上调并引发炎症反应。

结论

本研究证明SEA作为韩国人AD免疫炎症触发因子的重要性。

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