![]() |
JOURNAL TOOLS |
Publishing options |
eTOC |
To subscribe |
Submit an article |
Recommend to your librarian |
ARTICLE TOOLS |
Reprints |
Permissions |
Share |


YOUR ACCOUNT
YOUR ORDERS
SHOPPING BASKET
Items: 0
Total amount: € 0,00
HOW TO ORDER
YOUR SUBSCRIPTIONS
YOUR ARTICLES
YOUR EBOOKS
COUPON
ACCESSIBILITY
REVIEWS UPDATE ON CONTACT DERMATITIS
Giornale Italiano di Dermatologia e Venereologia 2007 December;142(6):639-48
Copyright © 2007 EDIZIONI MINERVA MEDICA
language: English
Impaired barrier function and the pathogenesis of atopic dermatitis
Jensen J. M., Fölster-Holst R., Proksch E.
Department of Dermatology University of Kiel, Kiel, Germany
A defect in barrier function is present in atopic dermatitis, potentially playing the causative role in the development of atopic lesions by enabling the penetration of type I environmental allergens into the skin, which consequently initiates immunological reactions and inflammation. This defect may be caused by genetic defects associated with the atopic syndrome (in particular filaggrin gene mutations) causing impaired nasal, bronchial, and intestinal mucous membranes. This leads to an enhanced penetration of environmental allergens such as those from house dust mite, cat dander and grass pollen into the skin which than leads to atopic dermatitis, allergic rhinitis, bronchial asthma. The immunological reaction results in increased epidermal proliferation and disturbed differentiation, accompanied by changes in lipid composition. Increased proliferation and disturbed differentiation have been identified in both lesional and non-lesional skin in atopic dermatitis. Because impaired epithelial defense appears to play a central role in the pathogenesis of atopic dermatitis, treatment strategies which address the long-term maintenance of barrier function by restoring lost lipid content and skin barrier hydration are of great importance for atopic patients.