Leung D Y, Harbeck R, Bina P, Reiser R F, Yang E, Norris D A, Hanifin J M, Sampson H A
Department of Pediatrics, National Jewish Center for Immunology and Respiratory Medicine, Denver, Colorado 80206.
J Clin Invest. 1993 Sep;92(3):1374-80. doi: 10.1172/JCI116711.
In the current study, we investigated whether Staphylococcus aureus grown from affected skin of atopic dermatitis (AD) patients secreted identifiable toxins that could act as allergens to induce IgE-mediated basophil histamine release. The secreted toxins of S. aureus grown from AD patients were identified by ELISA using antibodies specific for staphylococcal enterotoxin (SE) exfoliative toxin (ET), or toxic shock syndrome toxin (TSST-1). S. aureus isolates from 24 of 42 AD patients secreted identifiable toxins with SEA, SEB, and TSST accounting for 92% of the isolates. 32 of 56 AD sera (57%) tested contained significant levels of IgE primarily to SEA, SEB, and/or TSST. In contrast, although SEA, SEB, or TSST secreting S. aureus could be recovered from the skin of psoriasis patients, their sera did not contain IgE antitoxins. Freshly isolated basophils from 10 AD patients released 5-59% of total histamine in response to SEA, SEB, or TSST-1 but only with toxins to which patients had specific IgE. Basophils from eight other AD patients and six normal controls who had no IgE antitoxin failed to demonstrate toxin-induced basophil histamine release. Stripped basophils sensitized with three AD sera containing IgE to toxin released 15-41% of total basophil histamine only when exposed to the relevant toxin, but not to other toxins. Sensitization of basophils with AD sera lacking IgE antitoxin did not result in release of histamine to any of the toxins tested. These data indicate that a subset of patients with AD mount an IgE response to SEs that can be grown from their skin. These toxins may exacerbate AD by activating mast cells, basophils, and/or other Fc epsilon-receptor bearing cells armed with the relevant IgE antitoxin.
在本研究中,我们调查了从特应性皮炎(AD)患者患部皮肤分离出的金黄色葡萄球菌是否分泌可识别的毒素,这些毒素可作为变应原诱导IgE介导的嗜碱性粒细胞组胺释放。使用针对葡萄球菌肠毒素(SE)、剥脱毒素(ET)或中毒性休克综合征毒素(TSST-1)的特异性抗体,通过酶联免疫吸附测定(ELISA)鉴定从AD患者分离出的金黄色葡萄球菌所分泌的毒素。42例AD患者中有24例的金黄色葡萄球菌分离株分泌可识别的毒素,其中SEA、SEB和TSST占分离株的92%。56份AD血清中有32份(57%)检测发现主要针对SEA、SEB和/或TSST含有显著水平的IgE。相比之下,虽然从银屑病患者皮肤中可分离出分泌SEA、SEB或TSST的金黄色葡萄球菌,但其血清中不含IgE抗毒素。从10例AD患者新鲜分离的嗜碱性粒细胞对SEA、SEB或TSST-1刺激释放了5%-59%的总组胺,但仅对患者具有特异性IgE的毒素有反应。另外8例AD患者和6例无IgE抗毒素的正常对照的嗜碱性粒细胞未显示毒素诱导的嗜碱性粒细胞组胺释放。用含有针对毒素的IgE的3份AD血清致敏的脱颗粒嗜碱性粒细胞,仅在暴露于相关毒素时而不是其他毒素时,释放了15%-41%的总嗜碱性粒细胞组胺。用缺乏IgE抗毒素的AD血清致敏嗜碱性粒细胞不会导致对任何测试毒素的组胺释放。这些数据表明,一部分AD患者对可从其皮肤中培养出的SE产生IgE反应。这些毒素可能通过激活肥大细胞、嗜碱性粒细胞和/或其他携带相关IgE抗毒素的Fcε受体细胞而加重AD。