Abstract
Staphylococcus colonization is one of the aggravating factors in patients with atopic dermatitis. The Th2 inflammatory response and persistent IL-18 secretion from keratinocytes is induced by wall TA and protein A, respectively. Staphylococcus enterotoxins A (SEA) and B (SEB) stimulate the expression of ICAM-1 and HLA-DR in normal human keratinocytes, and more than half of patients with atopic dermatitis have specific IgE antibodies to SEA and/or SEB in their serum. Epicutaneous sensitization with SEB elicites a local, cutaneous inflammatory response characterized by dermal infiltration with eosinophils and mononuclear cells, and induces mRNA expression of the Th2 cytokine, IL-4 without increased expression of the Th1 cytokine, IFN-γ. Epicutaneous exposure to superantigens skews the immune response toward Th2, leading to allergic skin inflammation and increased IgE synthesis. Patients with atopic dermatitis have significantly increased numbers of regulatory T (Treg) cells with normal immunosuppressive activity. However, after superantigen stimulation, Treg cells lose their immunosuppressive activity. S.aureus, therefore, may aggravate atopic dermatitis by immunomudulatory effects of the cell components and exotoxins. Neither antimicrobial nor antiseptic treatment is effective for eradication of colonizing S.aureus in the horny layers covered with biofilm.
