Affiliations: Department of Pediatrics, University of Bologna,
Italy | Clinical and Experimental Medicine, Division of
Dermatology, University of Bologna, Italy
Note: [] Correspondence: Giampaolo Ricci, M.D., Department of Pediatrics,
University of Bologna, Via Massarenti 11, 40138 Bologna, Italy. Tel.: +39 051
6363075; Fax: +39 051 6364679; E-mail: [email protected]
Abstract: The skin of patients affected by atopic dermatitis (AD) is extremely
susceptible to colonization by Staphylococcus aureus, which plays
an important role in AD exacerbations and is correlated with AD extent and
severity. The mechanisms by which the bacterium colonizes and infects the skin
of patients with AD can be summarized by three different and subsequent steps:
1) a defective skin barrier, on which 2) S. aureus is able to adhere and
proliferate thanks to 3) the defective immune response of the skin. Several
S. aureus strains can secrete enterotoxins, which can act as
superantigens thus contributing to disease severity by inducing a polyclonal
T-cell activation and the release of proinflammatory cytokines such as
TNFα, IL-1β, IL-2. The
production of immunoglobulin E antibodies against staphylococcal exotoxins has
also been demonstrated, and the staphylococcal wall protein A has been
suggested to act as a "superallergen". Therapeutical actions against S.
aureus skin overinfection include both pharmacological (antimicrobial and/or
anti-inflammatory therapy and the newer topical calcineurin inhibitors) and
nonpharmacological treatments (silk fabric textiles), and are aimed at
minimizing skin colonization in order to reduce clinical exacerbations and AD
severity.
Keywords: Childhood eczema, atopic dermatitis, S. aureus, superantigens, superallergens
