| First Author | Lee NR | Year | 2020 |
| Journal | Sci Rep | Volume | 10 |
| Issue | 1 | Pages | 20237 |
| PubMed ID | 33214595 | Mgi Jnum | J:299999 |
| Mgi Id | MGI:6491089 | Doi | 10.1038/s41598-020-77281-x |
| Citation | Lee NR, et al. (2020) Role of 11beta-hydroxysteroid dehydrogenase type 1 in the development of atopic dermatitis. Sci Rep 10(1):20237 |
| abstractText | Glucocorticoids (GCs) are potent anti-inflammatory drugs, the secretion of which is mediated and controlled by the hypothalamic-pituitary-adrenal axis. However, they are also secreted de novo by peripheral tissues for local use. Several tissues express 11beta-hydroxysteroid dehydrogenase 1 (11beta-HSD1), including the skin. The inactive GC cortisone is converted by 11beta-HSD1 to active GC cortisol, which is responsible for delayed wound healing during a systemic excess of GC. However, the role of 11beta-HSD1 in inflammation is unclear. We assessed whether 11beta-HSD1 affects the development of atopic dermatitis (AD) in vitro and in vivo. The expression of 11beta-HSD1 in the epidermis of AD lesions was higher than that in the epidermis of healthy controls. Knockdown of 11beta-HSD1 in human epidermal keratinocytes increased the production of thymic stromal lymphopoietin. In an oxazolone-induced mouse model of AD, localized inhibition of 11beta-HSD1 aggravated the development of AD and increased serum cytokine levels associated with AD. Mice with whole-body knockout (KO) of 11beta-HSD1 developed significantly worse AD upon induction by oxazolone. We propose that 11beta-HSD1 is a major factor affecting AD pathophysiology via suppression of atopic inflammation due to the modulation of active GC in the skin. |
