Corticotropin-releasing hormone (CRH), a 41-amino-acid peptide, is a main regulator of the systemic response that suppresses immune response on a central level (Chrousos and Gold, 1992). In the peripheral sites, including the epidermis, CRH acts as potent proinflammatory agent (Karalis et al., 1991; Theoharides et al., 2004; Slominski et al., 2006a, b). In normal keratinocytes, CRH activates the master regulator of inflammation NF-κB (Zbytek et al., 2004) and stimulates the expression of ICAM-1 and HLA-DR (Quevedo et al., 2001).

Epidermal keratinocytes take part in inflammatory responses initiated by various stressors (Barker et al., 1991). Induction of production of inflammatory cytokines in normal keratinocytes by bacteria occurs via toll-like receptor (TLR)-2 and TLR-4 (Nagy et al., 2005). Therefore, there is a need for the functional study of the link between bacteria, CRH, and inflammatory cytokines in human keratinocytes.