Role of Antimicrobial Peptides in Skin Barrier Repair in Individuals with Atopic Dermatitis

• Published in: International journal of molecular sciences Vol. 21; no. 20; p. 7607
• Main Authors: Nguyen, Hai Le Thanh, Trujillo-Paez, Juan Valentin, Umehara, Yoshie, Yue, Hainan, Peng, Ge, Kiatsurayanon, Chanisa, Chieosilapatham, Panjit, Song, Pu, Okumura, Ko, Ogawa, Hideoki, Ikeda, Shigaku, Niyonsaba, François
• Format: Journal Article
• Language: English
• Published: Switzerland MDPI AG 14.10.2020; MDPI
• Subjects: Antiinfectives and antibacterials; Antimicrobial agents; antimicrobial peptide; Antimicrobial peptides; Asthma; Atopic dermatitis; barrier function; Barriers; Cathelicidins - metabolism; Defensins; Defensins - metabolism; Dermatitis; Dermatitis, Atopic - metabolism; Dermatitis, Atopic - pathology; Disruption; Eczema; epidermal barrier; Fatty acids; Filaggrin; Food allergies; Health risk assessment; Homeostasis; Humans; Immunology; Infections; Keratin; Lipids; Mutation; Pathogenesis; Pathogens; Peptides; Permeability; Proteins; Repair; Review; Roles; Septicemia; Skin; Skin - metabolism; Skin - pathology; skin barrier repair; Skin diseases; Skin Physiological Phenomena; Stratum corneum; Structure-function relationships; Tight junctions; Wound Healing; atopic dermatitis; skin barrier repair; antimicrobial peptide; epidermal barrier; filaggrin; barrier function
• ISSN: 1422-0067; 1661-6596; 1422-0067
• DOI: 10.3390/ijms21207607

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 b-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.