Abstract

The epidermis represents an essential barrier versus a broad range of exogenous stimuli. To form a functional epidermis, keratinocytes express filaggrin which plays a vital role in atopic dermatitis. However the relationship between filaggrin and other skin diseases remains unknown. In our study we chose 5 different common skin diseases and analyzed the expression of filaggrin in the skin using immunohistochemistry. Imiquimod (IMQ)-induced mouse model was used for detecting the filaggrin level and barrier function. The results indicated that the expression of filaggrin is reduced in psoriasis compared to the other skin diseases. Furthermore in vivo study showed that the skin barrier is defected with a decreased expression of filaggrin in IMQ-induced psoriasis mouse model, which is accompanied with an increased level of IL-17/IL-23. In conclusion, the defective skin barrier is involved in the development of psoriasis in human and mice with a reduced expression of filaggrin which may be regulated by the increased level of IL-17/IL-23 in the skin.

Highlights

  • The skin, as the largest organ in the body comprising approximately 10% of body weight, protects the body from dehydration and environmental insults through establishment of the protective epidermal permeability barrier

  • These results indicate that the skin barrier protein filaggrin is reduced in the psoriasis patients compared to normal healthy skin

  • Several skin disorders are associated with impaired skin barrier function, such as atopic dermatitis and other inflammatory skin diseases [4]

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Summary

Introduction

The skin, as the largest organ in the body comprising approximately 10% of body weight, protects the body from dehydration and environmental insults through establishment of the protective epidermal permeability barrier. The ectodermal cell layer covering the body develops into a stratified epidermis which is essential at birth and has the ability to confront the arid and toxic postnatal environments [3]. To maintain skin barrier homeostasis requires the delivery of lipids and proteins, which are contained in lamellar granules (keratinosomes) of the granular layer, to the stratum corneum interstices and the formation of high molecular weight polymers through the crosslinking of corneocyte envelope proteins such as loricrin, involucrin, filaggrin and other peptides. The epidermal barrier after birth is mainly regulated by a complex epidermal differentiation program [2]

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