Human skin is covered with microorganisms, but usually not infected. This is achieved apart from the physical skin barrier by a “chemical barrier,” consisting mainly of antimicrobial peptides (AMPs). Some of the AMPs are constitutively produced, among them are lysozyme, RNase 7 (R7) and to some extent psoriasin. Psoriasin (S100A7) is secreted from keratinocytes and preferentially kills Escherichia coli, thus protecting us from gram-negative gut bacterial infection. R7 is a major and broad-spectrum skin-AMP, which preferentially kills Enterococci thus controlling gram-positive gut bacterial growth at the skin surface. It is believed that these AMPs play a major role in the protection of healthy skin. When microbes come into contact with the living epidermis, e.g. by a defective physical barrier, these will induce additional AMPs like betadefensins. Human beta-defensin-2 (hBD-2) is the most abundant inducible and rather gram-negative bacteria-selective human peptide antibiotic, expressed in skin upon inflammation and infection. Apart from gram-negative bacteriaderived “pathogen-associated molecules”, proinflammatory cytokines have a high-capacity to induce hBD-2. The broad-spectrum AMP “human betadefensin-3 (hBD-3)” is selectively upregulated by growth factors and upon wound healing. Another inducible AMP is the cathelicidin-fragment Leu-Leu-37 (LL-37), a major AMP in neutrophils, which is also produced by keratinocytes during infection and inflammation. Therefore, human skin exhibits a wellstructured, multilayered antimicrobial defense system, where disturbance may lead to growth of pathogens and eventually infection.