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KMID : 0984920170190020050
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Journal of Skin Barrier Research
2017 Volume.19 No. 2 p.50 ~ p.51
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Improvement of Epidermal Function Prevents the Development of Psoriasis, Suggesting a Pathogenic Role of Epidermal Dysfunction
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Man Mao-Qiang
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Abstract
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Although psoriasis has long been considered as an immunologically-initiated disorder based on laboratory and clinical evidence, a line of evidence suggests that psoriasis could be ‘driven’ by a primary defect in epidermal function. The flare of psoriasis often occurs in lower humidity seasons and regions. Studies have shown that stratum corneum (SC) hydration is lower while basal transepidermal water loss rates and skin surface pH are higher during winter than during summer. Low SC hydration alone has substantial impact on cutaneous function, including induction of pruritus, stimulation of epidermal proliferation and cutaneous inflammation. Scratching resulting from low humidity-induced pruritus can cause further damage to the epidermal permeability barrier. Moreover, higher skin surface pH alone delays barrier recovery. During low humidity seasons, mechanical trauma, i.e, scratching and abrasion, induced barrier damage would be repaired more slowly due to the higher SC pH. Defective permeability barrier not only further increases SC pH, but also stimulates epidermal proliferation, cytokine production, inflammatory infiltration, as well as epidermal vascular endothelial growth factor production, leading to dermal capillary proliferation, all of which are prominent features of psoriasis. Furthermore, barrier disruption decreases expression levels of filaggrin and cornified envelope protein, resulting in a delay in permeability barrier repair. In normal subjects, the negative impact of exogenous stressors on epidermal function can be readily overcome or minimized. In contrast, in subjects bearing psoriasis susceptibility genes, alterations of epidermal function induced by exogenous stressors cannot be repaired rapidly, due to those genetic defects. A sustained barrier defect provokes excess keratinocyte proliferation and inflammation, leading to the development of psoriasis. Thus, psoriasis is likely due to permeability barrier-associated genetic defects and is triggered by external stressors. In support of this hypothesis of epidermal dysfunction, recently we and others have demonstrated that a) topical improvement
of epidermal function can prevent the development of psoriasis; b) combination of glucocorticoids and improvement of epidermal function can increase therapeutic efficacy; c) improvement of epidermal function benefits psoriasis during maintenance phase. In conclusion, epidermal dysfunction plays a pathogenic role in the development of psoriasis. Improvements of epidermal function could serve a valuable approach for preventing and treating psoriasis.
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