Abstract
Evidence is accumulating that skin can act as an independent steroidogenic organ. It can respond to various stresses including UV light, trauma and oncogenesis by upregulating glucocorticoid production via elements of the local hypothalamic-pituitary-adrenal (HPA) axis. Recent data by Takei and collaborators provided in this issue of Experimental Dermatology included dryness to the list of stressors stimulating cutaneous cortisol synthesis with a possible involvement of IL-1β as a mediator of this regulation. Thus, the last decade of research has not only documented that skin can produce cortisol, but that levels of its production change in response to environmental stress. The role of this regulated steroidogenic system in physiological or pathological outcomes requires further studies with focus on cutaneous homeostasis, formation of epidermal barrier, antimicrobial activity and display of immune (both pro- and anti-inflammatory) properties.