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葡萄球菌超抗原在特应性皮炎中的作用：对角质形成细胞的影响。

Role of staphylococcal superantigen in atopic dermatitis: influence on keratinocytes.

作者信息

Kim Kyu Han, Han Ji Hyun, Chung Jin Ho, Cho Kwang Hyun, Eun Hee Chul

机构信息

Department of Dermatology, Seoul National University College of Medicine, Clinical Research Institute, Seoul National University Hospital, Chongno-gu, Seoul, Korea.

出版信息

J Korean Med Sci. 2006 Apr;21(2):315-23. doi: 10.3346/jkms.2006.21.2.315.

DOI:10.3346/jkms.2006.21.2.315
PMID:16614521
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2734011/
Abstract

Staphylococcus aureus may perform an crucial function in atopic dermatitis (AD), via the secretion of superantigens, including staphylococcal enterotoxins (SE) A or B, and toxic shock syndrome toxin-1 (TSST-1). Dysregulated cytokine production by keratinocytes (KCs) upon exposure to staphylococcal superantigens (SsAgs) may be principally involved in the pathophysiology of AD. We hypothesized that lesional KCs from AD may react differently to SsAgs compared to nonlesional skin or normal skin from nonatopics. We conducted a comparison of HLA-DR or CD1a expression in lesional skin as opposed to that in nonlesional or normal skin by immunohistochemistry (IHC). We also compared, using ELISA, the levels of IL-1alpha, IL-1beta, and TNF-alpha secreted by cultured KCs from lesional, nonlesional, and normal skin, after the addition of SEA, SEB and TSST-1. IHC revealed that both HLA-DR and CD1a expression increased significantly in the epidermis of lesional skin versus nonlesional or normal skin in quite a similar manner. IL-1alpha, IL-1beta, and TNF-alpha secretion was also significantly elevated in the cultured KCs from lesional skin after the addition of SsAgs. Our results indicated that KCs from lesional skin appear to react differently to SsAgs and increased proinflammatory cytokine production in response to SsAgs may contribute to the pathogenesis of AD.

摘要

金黄色葡萄球菌可能通过分泌超抗原在特应性皮炎（AD）中发挥关键作用，这些超抗原包括葡萄球菌肠毒素（SE）A或B以及中毒性休克综合征毒素-1（TSST-1）。角质形成细胞（KC）在接触葡萄球菌超抗原（SsAg）后细胞因子产生失调可能主要参与了AD的病理生理学过程。我们推测，与非病变皮肤或非特应性个体的正常皮肤相比，AD病变部位的KC对SsAg的反应可能不同。我们通过免疫组织化学（IHC）比较了病变皮肤与非病变或正常皮肤中HLA-DR或CD1a的表达情况。我们还使用酶联免疫吸附测定（ELISA）比较了在添加SEA、SEB和TSST-1后，来自病变、非病变和正常皮肤的培养KC分泌的IL-1α、IL-1β和TNF-α水平。免疫组织化学显示，与非病变或正常皮肤相比，病变皮肤表皮中HLA-DR和CD1a的表达均以非常相似的方式显著增加。在添加SsAg后，来自病变皮肤的培养KC中IL-1α、IL-1β和TNF-α的分泌也显著升高。我们的结果表明，病变皮肤中的KC对SsAg的反应似乎不同，并且对SsAg产生的促炎细胞因子增加可能有助于AD的发病机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/48aa/2734011/20f63c94e422/jkms-21-315-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/48aa/2734011/77b7ae892979/jkms-21-315-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/48aa/2734011/59662705f236/jkms-21-315-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/48aa/2734011/1ef6125e4700/jkms-21-315-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/48aa/2734011/ad683fc32113/jkms-21-315-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/48aa/2734011/20f63c94e422/jkms-21-315-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/48aa/2734011/77b7ae892979/jkms-21-315-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/48aa/2734011/59662705f236/jkms-21-315-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/48aa/2734011/1ef6125e4700/jkms-21-315-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/48aa/2734011/ad683fc32113/jkms-21-315-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/48aa/2734011/20f63c94e422/jkms-21-315-g005.jpg

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