Matsunaga T, Katayama I, Yokozeki H, Nishioka K
Department of Dermatology, Tokyo Medical and Dental University School of Medicine, Japan.
J Dermatol Sci. 1996 Feb;11(2):104-10. doi: 10.1016/0923-1811(95)00426-2.
Bacterial superantigen such as staphylococcal enterotoxin B (SEB) induced strong ICAM-1 expression in organ-cultured human keratinocytes. Other superantigens (SEA, SEC1, SEC2) but not mite antigen (Dermatophagoides) also induced ICAM-1 expression both at protein and mRNA level. In contrast to ICAM-1, vascular endothelial cell expression of VCAM-1 was only demonstrated at mRNA level following ICAM-1 expression in keratinocytes. Patterns of cytokine expression in keratinocytes were variable. TNF alpha was strongly expressed in keratinocytes both at protein and mRNA level, while IL1 beta and IL1 alpha were only demonstrated at mRNA level. These results clearly demonstrated that bacterial superantigen could induce cell adhesion molecule expression in keratinocytes through the induction of various cytokines and play an important role in the induction of refractory eczematous lesions in atopic dermatitis.
诸如葡萄球菌肠毒素B（SEB）之类的细菌超抗原可在器官培养的人角质形成细胞中诱导细胞间黏附分子-1（ICAM-1）的强烈表达。其他超抗原（SEA、SEC1、SEC2）而非螨抗原（尘螨）也在蛋白质和mRNA水平上诱导ICAM-1表达。与ICAM-1不同，血管细胞黏附分子-1（VCAM-1）在角质形成细胞中ICAM-1表达后仅在mRNA水平上显示出血管内皮细胞表达。角质形成细胞中细胞因子的表达模式各不相同。肿瘤坏死因子α（TNFα）在蛋白质和mRNA水平上均在角质形成细胞中强烈表达，而白细胞介素1β（IL1β）和白细胞介素1α（IL1α）仅在mRNA水平上显示。这些结果清楚地表明，细菌超抗原可通过诱导各种细胞因子在角质形成细胞中诱导细胞黏附分子表达，并在特应性皮炎难治性湿疹样皮损的诱导中起重要作用。
