An international team led by NTU Singapore and the University of Geneva identified extracellular electron transport (EET) in Enterococcus faecalis as a mechanism that generates reactive oxygen species (ROS) to trigger the unfolded protein response in host epithelial cells, impairing wound closure. The preclinical work, published in Science Advances, linked bacterial redox metabolism directly to host cell stress and stalled healing in mice and human cell models. Co‑senior authors Guillaume Thibault and Kimberly Kline mapped how neutralizing EET restored epithelial migration and wound repair, suggesting a non‑antibiotic intervention point for chronic wounds complicated by antibiotic‑resistant E. faecalis. The paper emphasizes translational potential given the global burden of diabetic foot ulcers and other chronic wounds. Clarification: extracellular electron transport (EET) refers to microbial pathways that move electrons outside the cell, altering local redox chemistry. The study proposes targeting bacterial metabolism or downstream host stress responses as adjunct therapies to accelerate healing.