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      Diverse regulation of claudin-1 and claudin-4 in atopic dermatitis.

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          Abstract

          Tight junctions are important for skin barrier function. The tight junction protein claudin 1 (Cldn-1) has been reported to be down-regulated in nonlesional skin of atopic dermatitis (AD) patients. In contrast, we did not observe a significant down-regulation of Cldn-1 in nonlesional skin of the AD cohort used in this study. However, for the first time, a significant down-regulation of Cldn-1 in the upper and lower epidermal layers of lesional skin was detected. In addition, there was a significant up-regulation of Cldn-4 in nonlesional, but not lesional, AD skin. For occludin, no significant alterations were observed. In an AD-like allergic dermatitis mouse model, Cldn-1 down-regulation in eczema was significantly influenced by dermal inflammation, and significantly correlated with hallmarks of eczema (ie, increased keratinocyte proliferation, altered keratinocyte differentiation, increased epidermal thickness, and impaired barrier function). In human epidermal equivalents, the addition of IL-4, IL-13, and IL-31 resulted in a down-regulation of Cldn-1, and Cldn1 knockdown in keratinocytes resulted in abnormal differentiation. In summary, we provide the first evidence that Cldn-1 and Cldn-4 are differentially involved in AD pathogenesis. Our data suggest a role of Cldn-1 in AD eczema formation triggered by inflammation.

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          Author and article information

          Journal
          Am. J. Pathol.
          The American journal of pathology
          1525-2191
          0002-9440
          Oct 2015
          : 185
          : 10
          Affiliations
          [1 ] Department of Dermatology, Venerology, and Allergology, Medical University of Innsbruck, Innsbruck, Austria; Division of Human Genetics, Medical University of Innsbruck, Innsbruck, Austria. Electronic address: r.gruber@i-med.ac.at.
          [2 ] Department of Dermatology and Venerology, University Hospital Hamburg-Eppendorf, Hamburg, Germany.
          [3 ] Department of Medical Biometry and Epidemiology, University Hospital Hamburg-Eppendorf, Hamburg, Germany.
          [4 ] Department of Psychosomatic Medicine, Psychoneuroimmunology Laboratory, Justus-Liebig University, Giessen, Germany; Center for Internal Medicine and Dermatology, Charité-University Medicine, Berlin, Germany.
          [5 ] Department of Drug Delivery Technology, Leiden Academic Center for Drug Research, Leiden University, Leiden, the Netherlands.
          [6 ] Department of Dermatology, Venerology, and Allergology, Medical University of Innsbruck, Innsbruck, Austria; Division of Human Genetics, Medical University of Innsbruck, Innsbruck, Austria; Cologne Center for Genomics, University of Cologne, Cologne, Germany.
          [7 ] Department of Dermatology, Venerology, and Allergology, Medical University of Innsbruck, Innsbruck, Austria.
          [8 ] Department of Dermatology and Venerology, University Hospital Hamburg-Eppendorf, Hamburg, Germany. Electronic address: brandner@uke.de.
          Article
          S0002-9440(15)00427-7
          10.1016/j.ajpath.2015.06.021
          26319240
          c0811232-6a72-417a-a4be-d4a4abe69b7d
          Copyright © 2015 American Society for Investigative Pathology. Published by Elsevier Inc. All rights reserved.
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