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Presence of staphylococcal exfoliative toxin A in sera of patients with atopic dermatitis
Author(s) -
Yagi S.,
Wakaki N.,
Ikeda N.,
Takagi Y.,
Uchida H.,
Kato Y.,
Minamino M.
Publication year - 2004
Publication title -
clinical and experimental allergy
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.462
H-Index - 154
eISSN - 1365-2222
pISSN - 0954-7894
DOI - 10.1111/j.1365-2222.2004.1687.x
Subject(s) - superantigen , staphylococcus aureus , atopic dermatitis , enterotoxin , immunoglobulin e , immunology , exfoliative dermatitis , medicine , exacerbation , toxin , allergy , microbiology and biotechnology , antibody , dermatology , biology , immune system , bacteria , t cell , biochemistry , escherichia coli , gene , genetics
Summary Background It has been reported that the toxins that Staphylococcus aureus produces are associated with the exacerbation of atopic dermatitis (AD). It has been shown in many studies that staphylococcal enterotoxin (SE) A and SEB contribute to AD by humoral immunity through IgE production as a superantigen. On the other hand, little attention has been paid to the relationship between AD and exfoliative toxin x (ETx). Objective We investigated the toxins that are frequently detected from the skin of patients and how these toxins affect AD. Methods S. aureus , isolated from the skin of 100 patients with mild to severe AD, were examined for the producibility of toxins by polymerase chain reaction. Serum samples were obtained from 21 patients with mild and moderate AD. The levels of SEB, ETA, total IgE, specific IgE, and specific IgG in sera were measured by ELISA. Results SEB was most frequently detected from S. aureus on the skin of these patients as previously reported. And ETx, to which little attention has been paid so far, was frequently detected next to SEB. Furthermore, ETA was detected from the sera of almost all the AD patients. SEB was not detected at all. Although the level of ETA in the AD group was significantly higher than that of controls, ETA‐specific IgE was not detected from their sera. High levels of ETA tended to be detected from infantile patients. Although there were no significant differences in the levels of ETA‐IgG between AD and the controls, its prevalence was more than twice as high as the controls in AD. Conclusion These results suggest that many AD patients were exposed to ETx. We conclude that ETx may contribute to exacerbation of AD, particularly in infants, by a mechanism that is not through specific IgE production, unlike SEB.