Journal
ANNALS OF DERMATOLOGY
Volume 22, Issue 3, Pages 245-254Publisher
KOREAN DERMATOLOGICAL ASSOC
DOI: 10.5021/ad.2010.22.3.245
Keywords
Antimicrobial peptides; Atopic dermatitis; Barrier function; Barrier repair
Categories
Funding
- NIH [R01-AR019098, R01-AI059311]
- DOD [W81XWH-05-2-0094]
- Medical Research Service, Department of Veterans Affairs
Ask authors/readers for more resources
In this review, I first provide relevant background information about normal epidermal barrier structure and function. I then update recent information about how inherited defects in either filaggrin and/or in the serine protease inhibitor, lymphoepithelial Kazal-type inhibitor 1, converge to stimulate the development of atopic dermatitis (AD). Next I explain the multiple mechanisms whereby a primary barrier abnormality in AD can lead to inflammation. Furthermore, I explore how certain acquired stressors, such as a reduced external humidity, high pH soaps/surfactants, psychological stress, as well as secondary Staphylococcus aureus infections initiate or further aggravate AD. Finally, and most importantly, I compare various therapeutic paradigms for AD, highlighting the risks and benefits of glucocorticoids and immunomodulators vs. corrective, lipid replacement therapy. (Ann Dermatol 22(3) 245 similar to 254, 2010)
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