Epidermal dysfunctions in canine atopic dermatitis: Clinical impacts and therapies

Abstract

Canine atopic dermatitis (CAD) is an immune-mediated disease characterized by inflammatory and pruritic processes. Recent theories propose that epidermal barrier failures can facilitate the entry of potential allergens, microorganisms and irritants, increasing the interaction with cells of the immune system, causing its excessive stimulation. Therefore, the present review aims to describe the main epidermal changes that contribute to the pathogenesis of CAD, as well as to present therapies used to recover the skin barrier. The most frequent changes in the epidermis of atopic animals involve transepidermal water loss, lipid and protein dysfunctions. Ceramides are lipids with structural functions, but they are also involved in cell signaling. These molecules, although present, have reduced concentrations in the skin of dogs with CAD, which is considered both primary and secondary defects of inflammatory processes. Other epidermal components, such as filaggrin, an essential protein in development and maintenance of skin barrier integrity, and antimicrobial peptides responsible for defense against pathogens and modulation of immune response, have mutations in atopic animals, contributing to the appearance of recurrent infections. These defects in cutaneous barrier may contribute to the pathogenesis of CAD, and such information helps in the treatment of this pathology, improving animal welfare with skin-healing therapies.