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KMID : 0984920130150020093
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Journal of Skin Barrier Research
2013 Volume.15 No. 2 p.93 ~ p.94
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Corticosteroids, Psychological Stress, and Dermatitis
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Lin Tzu-Kai
Santiago Juan-Luis
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Abstract
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Dry environmental conditions induce a variety of pathological modifications in skin such as epidermal proliferation and inflammation, which are involved in the physiopathology of atopic dermatitis. Environmental dryness also induces cortisol secretion in the epidermis, which correlates with IL-1β synthesis in keratinocytes. This local production of cortisol might modulate inflammation and content the flares in chronic dermatitis. In fact, corticosteroids are widely used in the treatment of different inflammatory dermatoses by dermatologists. Psychological stress (PS) is well recognized to increase the plasma glucocorticoid (GC) levels in humans. Not only the stress-induced delay of barrier repair, but also the increase in plasma GC could be blocked by pretreatment with chlorpromazine, a tranquilizer. When mice were treated with the GC receptor antagonist, RU-486, baseline TEWL or barrier recovery rate were not altered. These results suggest that the stress-induced increase in GC might explain the impairment in skin barrier. Since increased endogenous GC production is induced by a variety of different stressors, including trauma, surgery, infection, and inflammation, it is likely that barrier homeostasis will be compromised in a wide variety of situations. Because PS has been preserved along evolution, there should be some advantage on health and survival. In fact, acute PS might provide some benefits decreasing the intensity of the early inflammatory response. Atopic dermatitis, psoriasis, and irritant dermatitis are the most common inflammatory dermatoses. All of them have been recently characterized as skin barrier disorders with a primary or secondary skin barrier defect. On the other hand, PS has been associated with exacerbation and propagation of some of them, such as psoriasis or atopic dermatitis. PS compromises both epidermal permeability and the expression of antimicrobial peptides (AMP). Systemic or topical corticosteroid (TCS) also decrease AMP levels in the epidermis, explaining the pathological mechanism involved in PS-induced skin barrier defects. According to these results, we should consider these negative effects on skin barrier when we use TCS in inflammatory dermatoses. In fact, even a short-term administration of either systemic or TCS to mice induced not only a delay in barrier recovery, but also abnormal stratum corneum integrity and cohesion. Thus, TCS might affect skin making it more vulnerable to a new inflammatory flare (e.g., rebound phenomenon), remarking the new interest about a more physiological approach in the management of chronic inflammatory dermatoses with skin barrier-repair therapies.
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