An NTU Singapore and University of Geneva team published in Science Advances that Enterococcus faecalis deploys extracellular electron transport (EET) to generate reactive oxygen species, activating the unfolded protein response in epithelial cells and impairing wound closure. The mechanistic work spans mouse models and human cell data and identifies EET as a virulence mechanism. Co-senior authors Guillaume Thibault and Kimberly Kline show that neutralizing the bacterial redox pathway restores epithelial migration in preclinical tests. With chronic wounds affecting millions and often complicated by antibiotic-resistant infections, targeting bacterial metabolism offers a non-antibiotic intervention pathway to improve healing outcomes.