Reduced expression of antimicrobial peptides was demonstrated for AD skin and favours colonization with S. aureus (Ong et al. N. Engl. J. Med. 2002; Howell et al.. Immunity. 2006;24:341-8; Rieg et al. JI 2006). In addition, dry skin may by itself allow colonization with bacteria such as S. aureus. Decreased levels of sphingosine, which has antimicrobial properties and the fact that S. aureus itself stimulates the hydrolysis of ceramides by bacterial derived ceramidase in atopic skin add the dysfunction of the immune barrier in AD (Arikawa et al., 2002; Kita et al, 2002). The cell membrane of S. aureus contains adhesins for epidermal and dermal laminin and fibronectin allowing attachemment of S. aureus. to the skin and these docking positions for S. aureus are uncovered in lesional skin (Cho et al, 2001). The precise mechanism by which S. aureus gains access to the dermis is unknown, but it is suggested that again IL-4, produced by T helper type 2 cells, induces fibronectin synthesis, which in combination with plasma exsudation of fibrinogen, allows S. aureus to bind to the skin. Moreover, S. aureus is able to encase itself in a kind of biofilm composed of a hydrated matrix of polysaccharides (glycocalix) and proteins, which supports cell adhesion (Akiyama et al., 2003). After colonization, S. aureus contributes to skin inflammation e.g. by secreting toxins and an array of so called pathogen associated molecular pattern (PAMP) that bind their pathogen recognition receptors such as Toll- like receptors and directly triggering inflammation (Biedermann 2006). Moreover, S. aureus PAMPs also influence T cell mediated skin inflammation by indirectly regulating skin homing of T cells and orchestrating chronic inflammation in AD skin (Biedermann 2006; Biedermann et al. 2006).