Role of Staphylococcal Superantigen in Atopic Dermatitis: Influence on Keratinocytes.
10.3346/jkms.2006.21.2.315
- Author:
Kyu Han KIM
1
;
Ji Hyun HAN
;
Jin Ho CHUNG
;
Kwang Hyun CHO
;
Hee Chul EUN
Author Information
1. Department of Dermatology, Seoul National University College of Medicine, Clinical Research Institute, Seoul National University Hospital and Institute of Dermatological Science Research, Seoul National University Medical Research Center, Seoul, Korea. ky
- Publication Type:Original Article ; In Vitro ; Research Support, Non-U.S. Gov't
- Keywords:
Dermatitis, Atopic;
Staphylococcal Superantigens;
Staphylococcal enterotoxin B;
HLA-DR Antigens;
Interleukin-1;
Tissue Necrosis Factor-alpha
- MeSH:
Tumor Necrosis Factor-alpha/biosynthesis/genetics;
*Superantigens/administration & dosage/immunology;
Staphylococcus aureus/*immunology/pathogenicity;
Male;
Keratinocytes/immunology/*microbiology;
Interleukin-1/biosynthesis/genetics;
Inflammation Mediators/metabolism;
Humans;
HLA-DR Antigens/metabolism;
Enterotoxins/administration & dosage/immunology;
Dermatitis, Atopic/etiology/immunology/*microbiology;
DNA, Complementary/genetics;
Case-Control Studies;
Base Sequence;
Bacterial Toxins/administration & dosage/immunology;
Antigens, CD1/metabolism;
Adult
- From:Journal of Korean Medical Science
2006;21(2):315-323
- CountryRepublic of Korea
- Language:English
-
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.
