Silk-derived sericin at the interface of atopic dermatitis and wound healing: Modulation of inflammation and epidermal repair

Title : Silk-derived sericin at the interface of atopic dermatitis and wound healing: Modulation of inflammation and epidermal repair

Abstract:

Atopic dermatitis (AD) is a chronic inflammatory skin disease characterized by immune dysregulation, epidermal barrier impairment, and defective tissue repair. Because mechanisms involved in barrier restoration overlap with those governing wound healing, biomaterials that simultaneously suppress inflammation and promote regeneration may offer particular therapeutic value. This study evaluated silk-derived sericin as a modulator of AD-associated inflammation and wound-repair pathways using complementary in vitro and in vivo models.

Sericin isolated from Bombyx mori cocoons was characterized by FTIR, SEM, and mass spectrometry. In vitro, human HaCaT keratinocytes, fibroblasts, and THP-1-derived macrophages were exposed to sericin, with inflammatory, barrier, and regenerative responses assessed by viability assays, scratch-wound analysis, RT-qPCR, and Western blotting. In keratinocytes, sericin at 600 µg/mL enhanced viability and migration, increased expression of repair-associated cytokeratins KRT16/KRT17 and the junctional protein JAM-A, and modulated inflammatory signaling. In fibroblasts, sericin promoted pro-remodeling and pro-angiogenic responses. In macrophages, sericin reduced IL-1β and TNF-α, increased IL-10, and favored an M2-like phenotype.

To assess translational relevance in AD, DNCB-induced dermatitis was established in rats and evaluated using clinical observation, histology, scratching behavior, and infrared thermography. Topical 2% sericin reduced erythema, normalized thermographic profiles, modulated inflammatory markers, and improved skin architecture compared with untreated lesions.

These findings indicate that sericin may bridge anti-inflammatory treatment of atopic dermatitis with activation of wound-healing and barrier-repair mechanisms. Its combined effects on keratinocyte migration, epithelial repair, macrophage polarization, and tissue inflammation support further development of sericin-based topical biomaterials for wound healing and inflammatory skin disorders associated with impaired barrier regeneration.

Grant Number: 2025/59/B/NZ4/00228

Biography:

Marek Konop, PhD, DSc, is an Associate Professor at the Medical University of Warsaw, Poland, working in the Department of Experimental Physiology and Pathophysiology. His research focuses on experimental dermatology, wound healing, regenerative medicine, and developing bioactive biomaterials for skin repair. His current work particularly explores keratin- and silk-derived biomaterials, including sericin, as modulators of inflammation, macrophage polarisation, and epidermal regeneration in acute and chronic wounds. He is also actively involved in international research collaborations, scientific publishing, and editorial activities in dermatology and regenerative medicine.