Colonization with superantigen-producing Staphylococcus aureus is associated with increased severity of atopic dermatitis.
BACKGROUND
Atopic dermatitis (AD) is a chronic inflammatory skin disease associated with colonization of the skin with Staphylococcus aureus known to produce toxins with superantigen (SAg) activity. Besides T-cell activation these toxins induce T-cell skin homing in vitro. This may contribute to the observed induction or enhancement of skin inflammation.


OBJECTIVE
The aim of this study was to determine whether colonization with SAg-producing S. aureus isolates modulates the intensity of AD. If so, it was of interest whether this may be primarily due to the toxins' effects as SAgs or as allergens.


METHODS
In AD patients, healthy controls, and atopic controls SAg production by S. aureus isolated from skin or mucous membranes was investigated and correlated to the severity of the disease. Total IgE, SAg-specific IgE, and T-cell activation and recirculation markers were analysed and correlated with SAg production.


RESULTS
Fifty-seven percent of S. aureus strains isolated from AD patients produced SAgs. This frequency was higher compared to healthy controls (33%). SAg production by S. aureus was correlated with a significantly higher scoring of AD (SCORAD index, 58 +/- 19 in SAg-producing vs 41 +/- 7 in non-SAg-producing germs; P < 0.05). However, the severity of the disease was not associated with sensitization against the SAgs staphylococcal enterotoxin A (SEA) and staphylococcal enterotoxin B (SEB). Furthermore, SAg production by S. aureus was inversely correlated with total IgE concentration (P < 0.05) and positively correlated with T-cell activation (as measured by HLA-DR and CD69 expression) and the expression of the T-cell skin homing phenotype cutaneous lymphocyte-associated antigen.


CONCLUSIONS
SAg production by S. aureus is suggested to be associated with an increased severity of atopic dermatitis. Since SAg production was found neither exclusively in AD patients nor in all patients, other pathogenic factors may be additionally effective.
Zollner
T M
TM
Department of Dermatology, University of Frankfurt Medical School, Theodor-Stern-Kai 7, D-60590 Frankfurt, Germany.
Wichelhaus
T A
TA
Hartung
A
A
Von Mallinckrodt
C
C
Wagner
T O
TO
Brade
V
V
Kaufmann
R
R
D000328:Adult; D000907:Antibodies, Bacterial / Q000276:immunology; D003876:Dermatitis, Atopic / Q000276:immunology* / Q000382:microbiology*; D005260:Female; D006801:Humans; D007073:Immunoglobulin E / Q000032:analysis; D008213:Lymphocyte Activation / Q000276:immunology; D008297:Male; D008875:Middle Aged; D009092:Mucous Membrane / Q000382:microbiology; D012720:Severity of Illness Index; D012867:Skin / Q000382:microbiology; D013211:Staphylococcus aureus / Q000276:immunology* / Q000302:isolation & purification; D018089:Superantigens / Q000276:immunology*; D013601:T-Lymphocytes / Q000276:immunology
D000907:Antibodies, Bacterial; D018089:Superantigens; D007073:Immunoglobulin E