Abstract
Atopic dermatitis (AD) is a common chronic inflammatory skin disease that exhibits a complex interplay of skin barrier disruption and immune dysregulation. Patients with AD are susceptible to cutaneous infections that may progress to complications, including staphylococcal septicemia. Although most studies have focused on filaggrin mutations, the physical barrier and antimicrobial barrier also play critical roles in the pathogenesis of AD. Within the physical barrier, the stratum corneum and tight junctions play the most important roles. The tight junction barrier is involved in the pathogenesis of AD, as structural and functional defects in tight junctions not only disrupt the physical barrier but also contribute to immunological impairments. Furthermore, antimicrobial peptides, such as LL-37, human β-defensins, and S100A7, improve tight junction barrier function. Recent studies elucidating the pathogenesis of AD have led to the development of barrier repair therapy for skin barrier defects in patients with this disease. This review analyzes the association between skin barrier disruption in patients with AD and antimicrobial peptides to determine the effect of these peptides on skin barrier repair and to consider employing antimicrobial peptides in barrier repair strategies as an additional approach for AD management.
Highlights
Atopic dermatitis (AD) is a highly prevalent, chronic inflammatory skin disease characterized by the complex interplay between skin barrier disruption and immune dysregulation [1,2,3]
Barrier repair therapy has focused on lipid replacement strategies in patients with AD, with a combination of ceramides, natural moisturizing factor (NMF), and pseudoceramide products added to therapeutic moisturizers
Studies investigating the application of these products in patients with AD have demonstrated their inconsistent efficacy
Summary
Atopic dermatitis (AD) is a highly prevalent, chronic inflammatory skin disease characterized by the complex interplay between skin barrier disruption and immune dysregulation [1,2,3]. In addition to the research characterizing FLG, the physical barrier and antimicrobial barrier have been determined to play crucial roles in the barrier-based pathogenesis of AD. Antimicrobial peptides (AMPs) are considered a rapid and first-line response of the innate immune system to microbial pathogens. Together with their antimicrobial effects, AMPs exert immunomodulatory effects by inducing cell migration, proliferation, and differentiation, regulating cytokine/chemokine production, improving angiogenesis and wound healing, and sustaining the barrier function of the skin [13,14]. Many advances in the understanding of skin barrier dysfunction in the pathogenesis of AD have been achieved, the treatment of this chronic disease remains unsatisfactory.
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