Premium
Expression patterns of superficial epidermal adhesion molecules in an experimental dog model of acute atopic dermatitis skin lesions
Author(s) -
Olivry Thierry,
Dunston Stanley M.
Publication year - 2015
Publication title -
veterinary dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.744
H-Index - 60
eISSN - 1365-3164
pISSN - 0959-4493
DOI - 10.1111/vde.12188
Subject(s) - desmosome , atopic dermatitis , transepidermal water loss , pathology , tight junction , immunostaining , medicine , house dust mite , stratum corneum , barrier function , desmoglein 3 , neutrophil elastase , immunology , immunohistochemistry , biology , allergen , allergy , inflammation , microbiology and biotechnology , autoimmune disease , genetics , disease , cell
Background The stratum corneum is critical for providing a functional skin barrier, especially in humans and dogs with atopic dermatitis. An effective barrier also depends upon intact corneodesmosomes and superficial epidermal tight junctions. Hypothesis/Objectives To study the expression of selected corneodesmosome, desmosome, tight and adherens junction proteins in an experimental model of acute atopic dermatitis skin lesions in dogs. Methods Control and house dust mite ( HDM ) allergen‐containing patches (two types of patches) were applied to the skin of six Maltese–beagle atopic dogs hypersensitive to HDM . Patches were left on for 48 h, and biopsies were collected 24 h after removal. Frozen skin sections were stained by indirect immunofluorescence for corneodesmosin, desmoglein‐1, desmocollin‐1, claudin‐1 and E‐cadherin. Immunostains were assessed for their extent, intensity and patterns; they were compared between HDM and control patches on the same dogs. Results The immunostaining for E‐cadherin, desmocollin‐1 and desmoglein‐1 was homogeneous, intercellular and continuous in all control and HDM patches. The immunoreactivity of corneodesmosin and claudin‐1 was heterogeneous and reduced in intensity in 12 of 12 and eight of 12 HDM patches, respectively, in contrast to a normal expression seen in all control samples (Fisher's test, P < 0.001). Conclusions and clinical importance These observations suggest that HDM allergens, via proteolytic digestion and/or because of induced allergic inflammation, affect the expression and possible function of corneodesmosomal and tight junction proteins. Ensuing intercellular junction alterations might promote an abnormally increased penetration of allergens through the epidermis.