Compared with normal skin, atopic skin is associated with increased adherence of S. aureus [1]. S. aureus infection probably results from a defect in skin barrier function and the loss of certain innate antibacterial activities [2]. S. aureus strains are part of the human nasal microbiome, and this carrier state has often been associated with type 2 immune responses including AD. S. aureus cell walls downregulate the human T cell response to superantigens through a TLR2-dependent, IL-10-mediated mechanism and prevent Th1 cell recruitment [3]. This evidence concerns the gene TLR2 and Alzheimer disease.