Psoriasis is characterized by keratino- cyte proliferation, inflammation, and mast cell activation (Schon and Boehncke, 2005). It is also triggered or exacerbated by acute stress (Katsarou- Katsari et al., 1999; Saraceno et al., 2006); however, this mechanism remains poorly understood. Stress typi- cally results in release of corticotropin- releasing hormone (CRH) from the hypothalamus and regulates the hy- pothalamic–pituitary–adrenal (HPA) axis (Chrousos, 1995) through activa- tion of CRH receptor-1 (CRH-R1), leading to immunosuppression. CRH is also found peripherally (Chrousos, 1995) and has pro-inflammatory effects through mast cell activation (Theohar- ides et al., 1998). CRH and CRH-R gene expression has been documented in rodent and human skin (Slominski et al., 2001). In fact, it has been proposed that skin has the equivalent of the HPA axis (Slominski et al., 2000). In mice, CRH is released from nerve endings (Slominski et al., 2001), whereas in humans it is synthesized by skin cells (Slominski et al., 1998), immune cells (Karalis et al., 1997), and human mast cells (Kempuraj et al., 2004).
