Escherichia coli infection induces ferroptosis in bovine mammary epithelial cells by activating the Wnt/β-catenin pathway-mediated mitophagy

•E. coli infection induced ferroptosis and mitophagy in bMECs.•E. coli infection inhibited activation of system Xc-/GPX4 axis in bMECs.•E. coli induced ferroptosis through Wnt/β-catenin pathway-mediated mitophagy. Iron overload causes mitochondrial damage, and then activates mitophagy, which may directly trigger and amplify ferroptosis. Our objective was to investigate whether Escherichia coli (E. coli) isolated from clinical bovine mastitis induces ferroptosis in bovine mammary epithelial cells (bMECs) and if so, the underlying regulatory mechanism. E. coli infection caused mitochondrial damage, mitophagy, and ferroptosis. Rapamycin and chloroquine increased and suppressed ferroptosis, respectively, in E. coli-treated bMECs. Moreover, E. coli infection activated the Wnt/β-catenin pathway, but foscenvivint alleviated it. In conclusion, E. coli infection induced ferroptosis through activation of the Wnt/β-catenin pathway-promoted mitophagy, and it also suppressed GPX4 expression.