title: Role of staphylococcal superantigen in atopic dermatitis: influence on keratinocytes.
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.
authors.affiliation: Department of Dermatology, Seoul National University College of Medicine, Clinical Research Institute, Seoul National University Hospital, Chongno-gu, Seoul, Korea. kyuhkim@snu.ac.kr
authors.forename: Kyu Han
authors.initials: KH
authors.lastname: Kim
authors.forename: Ji Hyun
authors.initials: JH
authors.lastname: Han
authors.forename: Jin Ho
authors.initials: JH
authors.lastname: Chung
authors.forename: Kwang Hyun
authors.initials: KH
authors.lastname: Cho
authors.forename: Hee Chul
authors.initials: HC
authors.lastname: Eun
mesh_terms: D000328:Adult; D018949:Antigens, CD1 / Q000378:metabolism; D001427:Bacterial Toxins / Q000008:administration & dosage / Q000276:immunology; D001483:Base Sequence; D016022:Case-Control Studies; D018076:DNA, Complementary / Q000235:genetics; D003876:Dermatitis, Atopic / Q000209:etiology / Q000276:immunology / Q000382:microbiology*; D004768:Enterotoxins / Q000008:administration & dosage / Q000276:immunology; D006684:HLA-DR Antigens / Q000378:metabolism; D006801:Humans; D066298:In Vitro Techniques; D018836:Inflammation Mediators / Q000378:metabolism; D007375:Interleukin-1 / Q000096:biosynthesis / Q000235:genetics; D015603:Keratinocytes / Q000276:immunology / Q000382:microbiology*; D008297:Male; D013211:Staphylococcus aureus / Q000276:immunology* / Q000472:pathogenicity; D018089:Superantigens / Q000008:administration & dosage / Q000276:immunology; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis / Q000235:genetics
chemical_list: D018949:Antigens, CD1; D001427:Bacterial Toxins; C419393:CD1a antigen; D018076:DNA, Complementary; D004768:Enterotoxins; D006684:HLA-DR Antigens; D018836:Inflammation Mediators; D007375:Interleukin-1; D018089:Superantigens; D014409:Tumor Necrosis Factor-alpha; C030107:enterotoxin F, Staphylococcal; C026066:enterotoxin A, Staphylococcal; C031818:enterotoxin B, staphylococcal