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Role of staphylococcal superantigen in atopic dermatitis: influence on keratinocytes

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Authors
Kim, Kyu Han; Han, Ji Hyun; Chung, Jin Ho; Cho, Kwang Hyun; Eun, Hee Chul
Issue Date
2006-04-15
Publisher
Korean Academy of Medical Science
Citation
J Korean Med Sci. 2006 Apr;21(2):315-23.
Keywords
AdultAntigens, CD1/metabolismBacterial Toxins/administration & dosage/immunologyBase SequenceCase-Control StudiesDNA, Complementary/geneticsDermatitis, Atopic/etiology/immunology/*microbiologyEnterotoxins/administration & dosage/immunologyHLA-DR Antigens/metabolismHumansInflammation Mediators/metabolismInterleukin-1/biosynthesis/geneticsKeratinocytes/immunology/*microbiologyMaleStaphylococcus aureus/*immunology/pathogenicity*Superantigens/administration & dosage/immunologyTumor Necrosis Factor-alpha/biosynthesis/genetics
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.
ISSN
1011-8934 (Print)
Language
English
URI
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=16614521

http://hdl.handle.net/10371/16288
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College of Medicine/School of Medicine (의과대학/대학원)Dermatology (피부과학전공)Journal Papers (저널논문_피부과학전공)
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