Backgrounds/Objectives: Skin wound healing is a physiological process orchestrated by epithelial and mesenchymal cells able to restore tissue continuity by re-organizing themselves and the ECM. This research study aimed to develop an optimized in vitro experimental model of full-thickness skin, to address molecular and morphological modifications occurring in the re-epithelization and wound healing process. Methods: Wound healing starting events were investigated within an experimental window of 8 days at the molecular level by gene expression and immunofluorescence of key epidermal and dermal biomarkers. To mirror the behavior of infected wounds, the established wound healing model was then colonized with S. aureus, and the efficacy of a novel antibacterial agent, XZ.700, was investigated. Viable counts (CFU/tissue), IF, and ultrastructural analysis (SEM) were performed to evaluate S. aureus colonization inside and around the wound bed in an experimental window of 3 h of colonization and 24 h of treatment. Results: Endolysin showed an efficacy in counteracting bacterial growth and invasion within the wound bed, reducing the S. aureus load compared to its placebo, thanks to its selective antimicrobial activity interfering with biofilm formation. Conclusions: The preclinical in vitro infected wound model on FT-kin showed interesting applications to assess the repair efficacy of dermo-pharmaceutical and cosmetic formulations.

Dry Eye Disease (DED) is a highly characterised multifactorial disease resulting in the loss of tear film homeostasis and associated with a major impact on patient quality of life. DED affects up to half of the global population, with modern lifestyle factors playing a critical role in disease development, particularly excessive use of digital devices. The ultimate treatment goal is restoration of tear film homeostasis and breaking the ‘vicious circle’ of DED. Today, the use of tear substitutes represents the main option for the treatment of DED. These topical formulations aim to provide lubrication, reduce osmolarity, and improve tear clearance. However, they do not interact with the ocular surface epithelium nor modulate ocular inflammation, and do not fully restore natural tear function. T-LysYal is the first supramolecular ocular surface modulator for DED. Studies demonstrate that T-LysYal promotes tissue repair, improves tear breakup time, restores corneal epithelial cell damage, and modulates inflammation processes, significantly reducing the severity of DED symptoms in patients. In addition, T-LysYal provides stability that prolongs activity and favours cell adhesion. Through its 3D nanotube structure, movement of water in the eye is retained and improved, enhancing ocular hydrodynamics. This narrative review introduces T-LysYal for DED whilst highlighting both its in vitro activity and clinical profile against hyaluronic acid, a mainstay of disease management.