Epidermal Barrier Dysfunction in Atopic Dermatitis

Abstract

Impaired skin barrier is one of the hallmarks of atopic dermatitis (AD), with abnormalities in the cornified envelope, lipid lamellae, tight junctions and cutaneous microbiome. These findings are also present in nonlesional skin of AD individuals, suggesting that epidermal barrier defects may be the initial step towards the development of AD and eventually other atopic diseases (atopic march). It is currently known that pathophysiology of AD involves an interplay between this dysfunctional skin barrier and a predominantly type 2 skewed innate and adaptive immune responses, which further disrupt the skin barrier through type 2 cytokines. In this setting, there is enhanced penetration of environmental and food allergens through a deficient barrier, leading to an increased susceptibility to sensitization. During the sensitization process, thymic stromal lymphopoietin (TSLP) polarizes skin dendritic cells to a T-helper 2 response, and TSLP seems to be a key cytokine in the sensitization of food allergy, allergic asthma and rhinitis. In this review, the authors describe the current knowledge of the pathophysiology of the epidermal barrier, its disruption in AD and how it may be involved in the development of atopic comorbidities and the role of barrier repair therapy on the prevention of the atopic march progression.

Should Emollients Be Recommended for the Prevention of Atopic Dermatitis?—New Evidence and Current State of Knowledge

“…One mentioned abnormality is mutations in the filaggrin gene (FLG), which is a major risk factor in the development of AD, along with a family history of atopy [6]. Mutations in the FLG increase the AD risk by 3-5 times [7]. Null mutations are observed in about half the patients with moderate-to-severe AD.…”

The cooperation between orf virus and Staphylococcus aureus leads to intractable lesions in skin infection

“…All kinds of virulence factors of S. aureus are frequently dealt with by the host (see Figure 2 ). If left unguarded, the destruction of the epidermal barrier may lead to protein loss and facilitate the cleavage of the corneodesmosome junctions ( Gomes et al., 2021) ), imbalance of body fluids and electrolytes, and increased risk of local and systemic infection. Therefore, S. aureus is more dangerous in destroying the microenvironment of host epithelium followed by sepsis and cytokine storm.…”