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Published on: March 19, 2018
New perspectives on epidermal barrier dysfunction in atopic dermatitis: gene-environment interactions
Michael J Cork1, Darren A Robinson, Yiannis Vasilopoulos
1Pediatric Dermatology Clinic, Children's Hospital, Sheffield S10 2RX, UK. m.j.cork@sheffield.ac.uk
Genetic factors and environmental triggers impair the skin barrier in atopic dermatitis (AD). This review highlights how epidermal barrier dysfunction exacerbates AD in genetically susceptible individuals.
Area of Science:
- Dermatology
- Immunology
- Genetics
Background:
- Atopic dermatitis (AD) is a chronic inflammatory skin disease influenced by genetics and environmental factors.
- While genetic mutations are implicated, their role in AD manifestation is often insufficient without other contributing factors.
Purpose of the Study:
- To propose a new perspective on the significance of epidermal barrier dysfunction in genetically predisposed individuals with AD.
- To explore how environmental agents interact with a compromised skin barrier to worsen AD.
Main Methods:
- This is a review article, synthesizing existing research on atopic dermatitis pathogenesis.
- Focuses on the role of epidermal barrier function, genetic predisposition, and environmental interactions.
Main Results:
- Genetic predisposition can lead to increased stratum corneum chymotryptic enzyme, prematurely breaking down corneodesmosomes and impairing the skin barrier.
- Environmental factors like soaps, detergents, topical corticosteroids, and exogenous proteases from mites and Staphylococcus aureus further damage the epidermal barrier.
- A defective skin barrier increases allergen penetration, leading to inflammation and AD exacerbations.
Conclusions:
- Epidermal barrier dysfunction is a critical factor in the pathogenesis of atopic dermatitis, particularly in genetically susceptible individuals.
- The interplay between genetic predisposition and environmental triggers significantly contributes to the chronic inflammatory cycle of AD.
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