PRESENCE OF IGE ANTIBODIES TO STAPHYLOCOCCAL EXOTOXINS ON THE SKIN OFPATIENTS WITH ATOPIC-DERMATITIS - EVIDENCE FOR A NEW GROUP OF ALLERGENS

Citation
Dym. Leung et al., PRESENCE OF IGE ANTIBODIES TO STAPHYLOCOCCAL EXOTOXINS ON THE SKIN OFPATIENTS WITH ATOPIC-DERMATITIS - EVIDENCE FOR A NEW GROUP OF ALLERGENS, The Journal of clinical investigation, 92(3), 1993, pp. 1374-1380
Citations number
34
Categorie Soggetti
Medicine, Research & Experimental
ISSN journal
00219738
Volume
92
Issue
3
Year of publication
1993
Pages
1374 - 1380
Database
ISI
SICI code
0021-9738(1993)92:3<1374:POIATS>2.0.ZU;2-E
Abstract
In the current study, we investigated whether Staphylococcus aureus gr own from affected skin of atopic dermatitis (AD) patients secreted ide ntifiable toxins that could act as allergens to induce IgE-mediated ba sophil histamine release. The secreted toxins of S. aureus grown from AD patients were identified by ELISA using antibodies specific for sta phylococcal enterotoxin (SE) exfoliative toxin (ET), or toxic shock sy ndrome toxin (TSST-1). S. aureus isolates from 24 of 42 AD patients se creted identifiable toxins with SEA, SEB, and TSST accounting for 92% of the isolates. 32 of 56 AD sera (57%) tested contained significant l evels of IgE primarily to SEA, SEB, and/or TSST. In contrast, although SEA, SEB, or TSST secreting S. aureus could be recovered from the ski n of psoriasis patients, their sera did not contain IgE antitoxins. Fr eshly isolated basophils from 10 AD patients released 5-59% of total h istamine in response to SEA, SEB, or TSST-1 but only with toxins to wh ich 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 sensitiz ed with three AD sera containing IgE to toxin released 15-41% of total basophil histamine only when exposed to the relevant toxin, but not t o other toxins. Sensitization of basophils with AD sera lacking IgE an titoxin did not result in release of histamine to any of the toxins te sted. These data indicate that a subset of patients with AD mount an I gE response to SEs that can be grown from their skin. These toxins may exacerbate AD by activating mast cells, basophils, and/or other Fceps ilon-receptor bearing cells armed with the relevant IgE antitoxin.