Format

Send to

Choose Destination
J Allergy Clin Immunol. 2000 Apr;105(4):814-9.

Evidence for a disease-promoting effect of Staphylococcus aureus-derived exotoxins in atopic dermatitis.

Author information

1
Charité Campus Virchow-Klinikum, Humboldt University of Berlin, Department of Pediatric Pneumology and Immunology, Berlin, Germany.

Abstract

BACKGROUND:

The skin of patients with atopic dermatitis (AD) exhibits a striking susceptibility to colonization with Staphylococcus aureus. Some strains of S aureus secrete exotoxins with T-cell superantigen activity (toxigenic strains), and abnormal T-cell functions are known to play a critical role in AD.

OBJECTIVE:

Our purpose was to examine the impact of superantigen production by skin-colonizing S aureus on disease severity.

METHODS:

In a cross-sectional study of 74 children with AD, the presence and density of toxigenic and nontoxigenic strains of S aureus was correlated with disease severity. In a subgroup of patients the T-cell receptor Vbeta repertoire of peripheral blood and lesional T cells was investigated and correlated with individual superantigen activity of skin-colonizing S aureus.

RESULTS:

Fifty-three percent of children with AD were colonized with toxigenic strains of S aureus producing staphylococcal enterotoxin C, staphylococcal enterotoxin A, toxic shock syndrome toxin-1, staphylococcal enterotoxin B, and staphylococcal enterotoxin D in decreasing frequency. Children colonized with toxigenic S aureus strains had higher disease severity compared with the nontoxigenic and S aureus-negative groups. Patients colonized with toxigenic S aureus exhibited shifts in the intradermal T-cell receptor Vbeta repertoire that correspond to the respective superantigen-responsive T-cell subsets.

CONCLUSION:

The data demonstrate that S aureus-released exotoxins can modulate disease severity and dermal T-cell infiltration.

PMID:
10756234
DOI:
10.1067/mai.2000.105528
[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Elsevier Science
Loading ...
Support Center