Abstract
Until recently, atopic dermatitis (AD) has been linked to Th1/Th2 cell dysregulation. But now, the opinion that inflammation in AD results from a convergence of inherited and acquired insults to the cutaneous permeability barrier, with variable contributions from inherited abnormalities in innate/adaptive immunity, is becoming increasingly accepted. Current therapy is however, still largely directed towards ameliorating immunologically triggered inflammation, rather than correcting the barrier abnormality. In this article, the authors provide an overview of epidermal barrier function; a review of recent molecular genetic studies pointing to a primary barrier abnormality in AD; a detailed description of new pathogenic insights into AD; and they compare the efficacy of several putative ‘barrier repair’ products currently utilized as adjunctive or primary therapy for AD. The authors also explore the potential of ‘next-generation’ barrier repair approaches that attack specific pathogenic mechanisms in AD (high surface pH, elevated serine protease activity, activation of the PAR2 receptor and Staphylococcus aureus secondary infections).
Financial & competing interests disclosure
PM Elias is a consultant for PuraCap Pharmaceutical LLC, the manufacturer of Epiceram, and a coinventor of triple-lipid based barrier repair therapy (patent held by the University of California, CA, USA). There was no industry support for this article. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.
No writing assistance was utilized in the production of this manuscript.
Notes
†C10/11 FFA are antimicrobial, but too short-chain to interact with membranes.
FFA: Free fatty acid.
Adapted with permission from Citation[104] © Future Science Group (2008).