skin barrier repair
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Novel magnesium doped non-mulberry silk fibroin nanofibers with ability to enhance skin barrier function were successfully fabricated using electrospinning technique for wound healing applications. Magnesium nanoparticles incorporated in the electrospun nanofibers releases Mg2+ ions at the site of implementation. The effect of Mg2+ is of considerable concern in wound healing due to its skin barrier repair ability and its role in blood coagulation. The physicochemical characterization of the scaffold was investigated by determining the morphology and secondary structure confirmation. The effects of Mg2+ ions in silk fibroin microenvironment have been evaluated using SEM, XRD, and FTIR to confirm the incorporation of magnesium in the film. The aim of this study is to see the effect of doped Mg on the structural, physical, and biological properties of non-mulberry silk fibroin (NSF) film. The magnesium doped nanofibrous film exhibited enhanced mechanical property, satisfactory blood clotting ability, and good in vitro degradability. This silk fibroin-based film mimicking extracellular matrix for skin regeneration were constructed using electrospinning technique. The wound healing efficiency of prepared nanofibers were evaluated in full-thickness wound models of rat. The Mg doped silk fibroin film exhibited faster wound healing activity (14 days) among all experimental group. The study indicates the potential of magnesium-doped silk /PVA film as skin substitute film.

Abstract not available.

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.