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
