Role of staphylococcal superantigens in atopic dermatitis: from colonization to inflammation.
OBJECTIVE
This review article has been prepared in order to enable the readers to understand the role of staphylococcal superantigens (SsAgs) in atopic dermatitis (AD).


METHODS
MEDLINE literature search was performed for obtaining references. Recent reviews, research articles, poster presentations, and letters (to the editor) were meticulously reviewed.


RESULTS
(1) SsAgs contribute to the pathogenesis of cutaneous inflammation in AD with five potential mechanisms: Direct stimulation of antigen presenting cells (APCs) and keratinocytes. Stimulation of T cell proliferation [superantigenic binding to T cell receptor (TCR)]. Expansion of skin-homing cutaneous lymphocyte antigen (CLA) (+) T cells. The role of superantigens as allergens. Reduction of apoptosis. (2) Effectiveness of antibiotic therapy in AD patients without signs of bacterial infection is still under discussion. If signs of skin infection are present, antibiotic therapy (topical/oral) may help exacerbations of AD. Prolonged topical/oral antibiotic therapy, however, may cause development of antibiotic-resistant strains of Staphylococcus aureus (SA).


CONCLUSIONS
Atopic dermatitis is a genetically determined, chronically relapsing, inflammatory skin disease which has many aspects and a complex immunopathogenesis involving both immediate and cellular immune responses. While the pathogenic role of SsAgs may not be of primary importance, SsAgs appear to be one of the important triggering factors that contribute to the cutaneous inflammation in AD. We suggest that staphylococcal colonization does not always mean SsAg-mediated inflammation, and anti-staphylococcal treatment should be considered in cases with signs of bacterial infection.
Taskapan
M O
MO
LSU Health Sciences Center, Dept. of Allergy & Clin. Immunology, Louisiana State University, School of Medicine, New Orleans 70112-2822, USA.
Kumar
P
P
D000818:Animals; D003876:Dermatitis, Atopic / Q000209:etiology* / Q000628:therapy; D006801:Humans; D011948:Receptors, Antigen, T-Cell / Q000502:physiology; D013210:Staphylococcus / Q000276:immunology*; D018089:Superantigens / Q000502:physiology*
D011948:Receptors, Antigen, T-Cell; D018089:Superantigens