Skin cells produce their own cortisol

The ability of our skin to maintain and repair its integrity is crucial to our survival. Upon wounding, an inflammatory response is initiated, followed by wound healing and regrowth of the skin layers, or skin epithelium. This inflammatory response is mediated by proteins including the cytokine interleukin-1 (IL-1) that occurs in the skin at the site of injury. IL-1 stimulates the production of glucocorticoids (cortisol) that are tasked to ward off any infiltrating foreign agents prior to initiation of wound repair.

Cortisol is a glucocorticoid steroid hormone that is released in when the immune response is in full swing. Until now, it has been thought that the adrenals were the only site of cortisol production. In this recent paper, Dr. S. Vukelic and colleagues (Journal of Biological Chemistry 286: 10265-10274, March 25, 2011) clearly demonstrate both in cell based (in vitro) and in animal based (in vivo) models that corticol synthesis occurs within the epithelium itself. This is the first evidence that local production of cortisol by specialized skin cells termed kertinocytes can control the local inflammatory response. Indeed, Vukelic et. al. demonstrate that keratinocytes contain the proper enzymes for corticol conversion from cholesterol precursors including CYP11B1, the cytochrome P450 gene necessary for the final conversion step to cortisol. The production of cortisol in keratintocytes is equivalent to that produced by the adrenals. Production peaks at 48 hours after injury and is followed by wound repair and skin regrowth.

This paper is significant because it suggests that local production of glucocorticoids may have clinical significance by influencing the rate of repair after injury.