An international team led by NTU Singapore and the University of Geneva published in Science Advances that Enterococcus faecalis impairs wound repair by generating reactive oxygen species via extracellular electron transport (EET). The EET-driven ROS activate the unfolded protein response (UPR) in epithelial cells, blocking migration and delaying closure in both mouse models and human cells. The authors—Guillaume Thibault and Kimberly Kline among them—demonstrated that neutralizing EET or its downstream effects restored epithelial migration and healing. The mechanism links bacterial redox metabolism directly to host-cell stress and offers a targetable virulence pathway for chronic wound infections, a major driver of diabetic foot complications worldwide.