An international team led by NTU Singapore and the University of Geneva reports in Science Advances that Enterococcus faecalis uses extracellular electron transport (EET) to generate reactive oxygen species (ROS), activating the unfolded protein response in epithelial cells and blocking wound closure. The preclinical work in mice and human cells links bacterial redox metabolism to persistent inflammation and impaired cell migration, identifying EET and downstream UPR activation as therapeutic entry points. Given the global burden of chronic wounds and antibiotic resistance, interventions that neutralize bacterial redox activity or modulate host UPR could restore healing without relying solely on antimicrobials. The paper nominates specific metabolic steps for drug discovery and adjunctive therapy development.