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KMID : 0984920170190020052
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Journal of Skin Barrier Research
2017 Volume.19 No. 2 p.52 ~ p.52
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Psychological Stress Deteriorates Skin Barrier Function by Activating 11β-Hydroxysteroid Dehydrogenase 1 and the HPA Axis
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Choe Sung-Jay
Kim Dong-Hye
Kim Eun-Jung
Ahn Joung-Sook
Choi Eun-Jeong
Son Eui-Dong
Lee Tae-Ryong
Choi Eung-Ho
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Abstract
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Psychological stress (PS) increases levels of endogenous glucocorticoids (GC) by activating the hypothalamic-pituitary-adrenal axis. The negative effects of PS on skin barrier function are well-established. However, endogenous GC can exert their activity when cortisone (inactive form) is converted into cortisol (active form) by 11β-hydroxysteroid dehydrogenase type I (11ß-HSD1) in peripheral tissues. Here, we evaluated changes in 11ß-HSD1 and barrier function in response to PS. Elevated 11ß-HSD1 in oral mucosa correlated with increased cortisol in the stratum corneum and deterioration of barrier function in medical students under PS. We also found that 11ß-HSD1 expression in oral mucosal cells correlated with that of epidermal keratinocytes. We demonstrated that 11ß-HSD1 is important for increasing cortisol in the keratinocytes because cortisol increase was attenuated upon knockdown of 11ß-HSD1 in cell culture and upon applying a topical 11ß-HSD1 inhibitor in skin organ culture. We further investigated whether barrier function improved when PS was relieved by selective serotonin reuptake inhibitor (SSRI) treatment in patients with anxiety. Decreased 11ß-HSD1 levels and improved barrier function were observed after SSRI treatment. These findings suggest that elevated 11ß-HSD1 under PS increases local GC levels, eventually impairs barrier function, and PS-alleviating drugs such as SSRIs may help treat PS-aggravated skin diseases.
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