Abstract
There is now considerable evidence that colonization or infection with Staphylococcus aureus is an exacerbating factor in atopic dermatitis (AD) (1). Numerous studies have shown that the superantigens produced by staphylococci and streptococci are implicated in the pathogenesis of various inflammatory skin diseases. The skin lesions of patients with AD predominantly contain infiltrating T cells and monocyte/macrophages which can be activated by superantigenic toxins from these microbes. This review focuses on two specific aspects of the involvement of S. aureus in AD. These are mechanisms by which superantigens can induce skin inflammation and impair the response of the inflammatory process to corticosteroids, and the inability of the innate immune system in atopic skin to counteract staphylococcal skin colonization and infection.
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