Nissen D, Pedersen L J, Skov P S, Vejlsgaard G L, Poulsen L K, Jarløv J O, Karlsmark T, Nolte H
Laboratory of Medical Allergology, National University Hospital, Copenhagen, Denmark.
Ann Allergy Asthma Immunol. 1997 Nov;79(5):403-8. doi: 10.1016/s1081-1206(10)63033-5.
The exacerbation of atopic dermatitis may be associated with infection of the skin with Staphylococcus aureus (S.aureus). S. aureus isolated from the skin of patients with atopic dermatitis secretes enterotoxin A, B, and toxic shock syndrome toxin 1. This is of interest because these patients may develop specific IgE antibodies against components from staphylococci.
The objective was to demonstrate IgE-sensitization to components of Staphylococcus aureus enterotoxins A and B (purified and partially purified), toxic shock syndrome toxin 1, and the bacterial cell component lipoteichoic acid, in patients with atopic dermatitis.
Blood samples from 34 patients with atopic dermatitis and 10 controls were tested by leukocyte histamine release to the enterotoxins and lipoteichoic acid. The toxins were separated by sodium dodecylsulfate polyacrylamide gel electrophoresis and analyzed by IgE-immunoblotting with sera from the same patients.
The majority of patients (96%) with clinical signs of skin infection produced specific IgE-antibodies to all three toxins. Nearly half of the patients produced IgE to enterotoxin A and B. Only 63% of the patients with atopic dermatitis showed cellular response judged by the release of histamine from patient basophils when challenged in vitro with the toxins. This may indicate clinically unimportant sensitization in a number of patients. The immunoblotting revealed that the major allergens of the toxins were 24 and 28 kD proteins. Partially purified toxins showed a higher frequency of leukocyte histamine release responses than purified toxin. The only obvious difference was a difference in the content of pure toxin of the two preparations. Lipoteichoic acid showed nonspecific activity.
These findings suggest that staphylococcal enterotoxins may act as specific allergens and induce IgE-antibodies to enterotoxins that may exacerbate the skin inflammation in some patients with atopic dermatitis.
特应性皮炎的加重可能与皮肤感染金黄色葡萄球菌(金葡菌)有关。从特应性皮炎患者皮肤分离出的金葡菌可分泌肠毒素A、B以及中毒性休克综合征毒素1。这一点值得关注,因为这些患者可能会产生针对葡萄球菌成分的特异性IgE抗体。
旨在证实特应性皮炎患者对金黄色葡萄球菌肠毒素A和B(纯化和部分纯化的)、中毒性休克综合征毒素1以及细菌细胞成分脂磷壁酸存在IgE致敏。
采用白细胞组胺释放试验检测34例特应性皮炎患者和10例对照者的血液样本对肠毒素和脂磷壁酸的反应。毒素经十二烷基硫酸钠聚丙烯酰胺凝胶电泳分离,并用同一患者的血清进行IgE免疫印迹分析。
大多数有皮肤感染临床症状的患者(96%)产生了针对所有三种毒素的特异性IgE抗体。近一半的患者产生了针对肠毒素A和B的IgE。只有63%的特应性皮炎患者在体外用毒素激发时,其嗜碱性粒细胞释放组胺,显示出细胞反应。这可能表明许多患者存在临床上无重要意义的致敏。免疫印迹显示,毒素的主要过敏原是24kD和28kD的蛋白质。部分纯化的毒素比纯化毒素显示出更高频率的白细胞组胺释放反应。唯一明显的差异是两种制剂中纯毒素的含量不同。脂磷壁酸显示出非特异性活性。
这些发现表明,葡萄球菌肠毒素可能作为特异性过敏原,诱导产生针对肠毒素的IgE抗体,这可能会加重一些特应性皮炎患者的皮肤炎症。