Atopic dermatitis (AD) is characterized by skin infiltration with eosinophils and lymphocytes and expression of Th₂ cytokines in acute skin lesions. The skin of patients with AD is frequently colonized with enterotoxin-secreting strains of Staphylococcus aureus. Staphylococcal enterotoxins have been implicated in the exacerbations of the inflammatory skin lesions in patients with AD.

We sought to determine whether epicutaneous (EC) sensitization of mice with staphylococcal enterotoxin B (SEB) results in allergic skin inflammation.

BALB/c mice were EC-sensitized with SEB. Their skin was examined for allergic inflammation and cytokine expression, and their splenocytes were examined for cytokine secretion in response to SEB.

EC sensitization with SEB elicited a local, cutaneous, inflammatory response characterized by dermal infiltration with eosinophils and mononuclear cells and increased mRNA expression of the Th₂ cytokine IL-4 but not of the Th₁ cytokine IFN-γ. EC-sensitized mice mounted a systemic Th₂ response to SEB evidenced by elevated total and SEB-specific IgG1 and IgE. Although EC sensitization with SEB resulted in selective depletion of SEB-specific T-cell receptor Vβ8+ cells from the spleen and sensitized skin, splenocytes from SEB-sensitized mice secreted relatively more IL-4 and less IFN-γ than did saline-sensitized controls, consistent with Th₂ skewing of the systemic immune response to the superantigen.

These results suggest that EC exposure to superantigens skews the immune response toward Th₂ cells, leading to allergic skin inflammation and increased IgE synthesis that are characteristic of AD.