Recent clinical trials have established a central role for the Th2 cytokines IL-4 and IL-13 in the pathology of atopic dermatitis (AD)(Beck et al., 2014). Although blockade of the IL-4 and IL-13 receptors causes significant clearing of skin lesions, a direct effect of Th2 cytokines on wound healing processes has not yet been demonstrated. Furthermore, AD patients are frequently affected by infection with the pathogen, Staphylococcus aureus (Boguniewicz and Leung, 2011). Elevated levels of staphylococcal products are frequently found on the skin of affected patients (Travers et al., 2010), and these products may affect the wound healing process as well.

A primary event in skin healing is induction of matrix metalloproteinases (MMPs)(Inoue et al., 1995). MMPs-1, 9, and 10 are expressed at the leading edge of the wound (Inoue et al., 1995; Rechardt et al., 2000; Turchi et al., 2003) and are required for keratinocyte migration into the damaged area (Agren, 1999; Pilcher et al., 1997). Inhibition of MMP function effectively blocks keratinocyte migration and wound healing (Mirastschijski et al., 2002b). However, over expression of MMPs has been reported in skin diseases, and can inhibit wound closure as well (Mirastschijski et al., 2002a; Saarialho-Kere et al., 1994). In this study, we determined the effects of staphylococcal products and AD associated Th2 cytokines on MMP expression and on keratinocyte migration.