The epidermal immune microenvironment is a multifaceted system in which the interplay between the skin microbiome and antimicrobial peptides plays a pivotal role in sustaining skin homeostasis and preventing dysbiosis. Disruption of these interactions can lead to inflammatory skin conditions such as atopic dermatitis. This review aims to explore the complex mechanisms by which antimicrobial peptides and the skin microbiome communicate within the epidermal immune microenvironment, emphasizing causal dynamics and the dual role of antimicrobial peptides.
View Article and Find Full Text PDFWound healing is a complex, multiphase process crucial for restoring tissue integrity and functionality after injury. Among the emerging therapeutic approaches, antimicrobial peptides (AMPs) have shown substantial promise because of their dual role in microbial defense and cellular modulation. AMP-IBP5, a novel AMP derived from insulin-like growth factor-binding protein 5, exhibits both antimicrobial and wound-healing properties, making it a promising therapeutic candidate.
View Article and Find Full Text PDFIntroduction: Atopic dermatitis (AD) is a chronic inflammatory skin disease characterized by pruritus, immune dysregulation, and compromised skin barrier function. Although there are some reports that indicate a link between AD and chronic kidney disease (CKD), the prevalence and underlying mechanism of the association between AD and CKD are still unclear. We aimed to clarify the mechanism underlying the association between AD and CKD using an AD-like mouse model.
View Article and Find Full Text PDFBackground: Atopic dermatitis (AD), a prevalent chronic inflammatory skin disorder, is characterized by compromised skin barrier and heightened immune responses. The study investigates the therapeutic efficacy of catestatin (CST), a chromogranin A-derived antimicrobial peptide, in mitigating AD-like symptoms.
Methods: Utilizing both keratinocyte cultures and a C57BL/6 mouse model, we examined CST's impact on skin barrier proteins, tight junction (TJ) integrity, inflammatory cytokines, and AD-like symptoms.