The role of Staphylococcus aureus in atopic eczema

Staphylococcus aureus infection plays an important role in atopic eczema (AE) because of its ability to produce virulence factors such as superantigens. Epicutaneous application of superantigens induces eczema. Superantigens also induce corticosteroid resistance, and subvert T-regulatory cell activity, thereby increasing AE severity. Increased binding of S. aureus to skin is driven by underlying AE skin inflammation. This is supported by studies demonstrating that treatment with topical corticosteroids reduces S. aureus counts on atopic skin. AE has also been found to be deficient in antimicrobial peptides needed for host defence against bacteria. The reduced production of antimicrobial peptides in AE appear to be an acquired defect resulting from increased T-helper type 2 cell (Th2) cytokine production. A vicious cycle of skin barrier dysfunction, skin infection and Th2 cell immune activation therefore occurs in AE. Effective strategies for controlling AE require combination therapy that reduces skin inflammation and controls S. aureus colonization and infection.