Abstract
Acne vulgaris is the result of multifactorial disorders of the pilosebaceous duct. The initial lesion is believed to be hyper-keratinization of the infundibulum. The Rhino mouse has been used as an experimental acne model system for screening anti-keratinizing and comedolytic agents. Using this system we show that trypsin could induce desquamation and utriculi-epidermal differentiation in the absence of irritation. Following five daily trypsin treatments, the biomechanical properties of the mouse skin improved, as demonstrated by cutometer measurements and increased elastin expression. Extensive programmed cell death and apoptosis are demonstrated in the utriculi epithelium of the untreated animals. This cell death is eliminated by the trypsin treatment. We speculate that co-administration of trypsin might increase the therapeutic value of topical acne treatments and improve skin elasticity while reducing irritating effects.
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