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KMID : 0984920090110020070
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Journal of Skin Barrier Research
2009 Volume.11 No. 2 p.70 ~ p.79
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Skin barrier alteration under psychological stress
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Choi Eung-Ho
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Abstract
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Atopic dermatitis and psoriasis are adversely affected by psychological stress (PS), but the pathophysiologic link between PS and disease expression remains unclear. Some series of recent studies showed that PS decreases epidermal proliferation and differentiation, impairs permeability barrier homeostasis, decreases stratum corneum (SC) integrity and increases group A Streptococcal pyogenes cutaneous infection in mice. PS also increases the production of endogenous glucocorticoids (GC), and both systemic and topical GC cause adverse effects on epidermal structure and function similar to those observed with PS. By the mechanisms PS decreases epidermal cell proliferation, impairs epidermal differentiation, decreases the density and size of corneodesmosomes (CD), and decreases an expression of epidermal antimicrobial peptide (AMP). Barrier dysfunction is resulted from decreased production and secretion of lamellar bodies (LB), which in turn, could be attributed to a decrease of epidermal lipid synthesis. Topical physiologic lipids mixture composed of equimolar cholesterol, ceramides and free fatty acids, normalized barrier homeostasis, SC integrity and AMP level in PS mice. Therefore, PS inhibition of epidermal lipid synthesis results in decreased LB production and secretion, as
well as decreased CD and AMP delivery to LB, which are compromising permeability barrier homeostasis, SC integrity and antimicrobial defense. To confirm the hypothesis that increased endogenous GC in PS mediates its adverse cutaneous effects, RU-486 and antalarmin were used. RU-486, a GC receptor antagonist, inhibits GC action, and antalarmin, a corticotropin releasing hormone (CRH) receptor antagonist, prevents increased GC production in the face of
PS. Inhibition of either GC action or production prevents the PS-induced decline in keratinocyte proliferation and differentiation, impairment in permeability barrier homeostasis, decrease in SC integrity and decrease of AMP expression. Thus, many of the adverse effects of PS on the structure and function of epidermal permeability and antimicrobial barrier can be attributed to increased endogenous GC. Conversely, approaches that either reduces GC production or action
might benefit skin diseases provoked or exacerbated by PS. Physiologic lipid replacement, PS reduction such as aroma therapy and meditation, and GC receptor antagonists could also be beneficial in PS induced, barrier associated dermatoses.
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KEYWORD
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Skin barrier, Psychological stress, Corticosteroid
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