Research Summary
Atopic dermatitis (AD) is a common chronic inflammatory skin disease characterized by 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 are of utmost importance. The tight junction barrier is particularly 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, have been shown to improve tight junction barrier function.
Recent studies elucidating the pathogenesis of AD have led to the development of barrier repair therapy for addressing skin barrier defects in patients with this condition. 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. It also considers the potential of employing antimicrobial peptides in barrier repair strategies as an additional approach for managing AD.
Keywords: antimicrobial peptide; atopic dermatitis; barrier function; epidermal barrier; filaggrin; skin barrier repair.
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