Psychological Stress Perturbs Epidermal Permeability Barrier Homeostasis

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Abstract
Background A large number of skin diseases, including atopic dermatitis and psoriasis,appear to be precipitated or exacerbated by psychological stress. Nevertheless,the specific pathogenic role of psychological stress remains unknown. In 3different murine models of psychological stress, it was recently shown thatpsychological stress negatively impacts cutaneous permeability barrier functionand that coadministration of tranquilizers blocks this stress-induced deteriorationin barrier function. Objectives and Methods The relationship between psychological stress and epidermal permeabilitybarrier function was investigated in 27 medical, dental, and pharmacy studentswithout coexistent skin disease. Their psychological state was assessed with2 well-validated measures: the Perceived Stress Scale and the Profile of MoodStates. Barrier function was assessed simultaneously with the stress measuresat periods of presumed higher stress (during final examinations) and at 2assumed, lower stress occasions (after return from winter vacation [approximately4 weeks before final examinations] and during spring vacation [approximately4 weeks after final examinations]). Results The subjects as a group demonstrated a decline in permeability barrierrecovery kinetics after barrier disruption by cellophane tape stripping, inparallel with an increase in perceived psychological stress during the highervs the initial lower stress occasions. During the follow-up, presumed lowerstress period, the subjects again displayed lower perceived psychologicalstress scores and improved permeability barrier recovery kinetics, comparableto those during the initial lower stress period. Moreover, the greatest deteriorationin barrier function occurred in those subjects who demonstrated the largestincreases in perceived psychological stress. Conclusion These studies provide the first link between psychological status andcutaneous function in humans and suggest a new pathophysiological paradigm,ie, stress-induced derangements in epidermal function as precipitators ofinflammatory dermatoses.

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