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Review
. 2018 May;10(3):207-215.
doi: 10.4168/aair.2018.10.3.207.

Significance of Skin Barrier Dysfunction in Atopic Dermatitis

Byung Eui Kim  1 , Donald Y M Leung  2
Affiliations
Review

Significance of Skin Barrier Dysfunction in Atopic Dermatitis

Byung Eui Kim et al. Allergy Asthma Immunol Res. 2018 May.

Abstract

The epidermis contains epithelial cells, immune cells, and microbes which provides a physical and functional barrier to the protection of human skin. It plays critical roles in preventing environmental allergen penetration into the human body and responsing to microbial pathogens. Atopic dermatitis (AD) is the most common, complex chronic inflammatory skin disease. Skin barrier dysfunction is the initial step in the development of AD. Multiple factors, including immune dysregulation, filaggrin mutations, deficiency of antimicrobial peptides, and skin dysbiosis contribute to skin barrier defects. In the initial phase of AD, treatment with moisturizers improves skin barrier function and prevents the development of AD. With the progression of AD, effective topical and systemic therapies are needed to reduce immune pathway activation and general inflammation. Targeted microbiome therapy is also being developed to correct skin dysbiosis associated with AD. Improved identification and characterization of AD phenotypes and endotypes are required to optimize the precision medicine approach to AD.

Keywords: Atopic dermatitis; antimicrobial peptide; epidermal barrier; microbiome; moisturizer.

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Conflict of interest statement

There are no financial or other issues that might lead to conflict of interest.

Figures

Fig. 1
Fig. 1. Impaired skin barrier enhances allergen penetration and activates the innate immune system. Multiple factors, including immune dysregulation, defects in terminal epithelial differentiation such as lack of filaggrin (FLG), deficiency of antimicrobial peptides (AMPs), altered composition of stratum corneum intercellular lipids, and altered skin microbiome cause skin barrier defects. Source: Czarnowicki et al. J Allergy Clin Immunol 2017;139:1723–34.
Fig. 2
Fig. 2. Keratinocytes differentiated in the presence of IL-4 and IL-13 exhibit significantly reduced filaggrin. Primary human keratinocytes were cultured for 5 days in 0.06 or 1.3 mmol/L CaCl2 in the presence of IL-4 plus IL-13 or interferon (IFN)-gamma. *P<0.05; ***P<0.001 between the exposure groups. Source: Howell et al. J Allergy Clin Immunol 2007;120:150–5.
See this image and copyright information in PMC

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