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Mammary pathogenic  Escherichia coli  (MPEC) is an important causative agent of mastitis in dairy cows that results in reduced milk quality and production, and is responsible for severe economic losses in the dairy industry worldwide. Oxidative stress, as an imbalance between reactive oxygen species (ROS) and antioxidants, is a stress factor that is common in most bacterial habitats. The presence of ROS can damage cellular sites, including iron-sulfur clusters, cysteine and methionine protein residues, and DNA, and may cause bacterial cell death. Previous studies have reported that Autoinducer 2 (AI-2) can regulate  E. coli  antibiotic resistance and pathogenicity by mediating the intracellular receptor protein LsrR. This study explored the regulatory mechanism of LsrR on the H 2 O 2  stress response in MPEC, showing that the transcript levels of  lsrR  significantly decreased under H 2 O 2  stress conditions. The survival cell count of  lsrR  mutant XW10/pSTV28 was increased about 3080-fold when compared with that of the wild-type WT/pSTV28 in the presence of H 2 O 2  and overexpression of  lsrR  (XW10/pUClsrR) resulted in a decrease in bacterial survival rates under these conditions. The β-galactosidase reporter assays showed that mutation of  lsrR  led to a remarkable increase in expression of the promoters of  ahpCF ,  katG  and  oxyR , while  lsrR -overexpressing significantly reduced the expression of  ahpCF  and  katG . The electrophoretic mobility shift assays confirmed that LsrR could directly bind to the promoter regions of  ahpCF  and  katG . These results revealed the important role played by LsrR in the oxidative stress response of MPEC .

LsrR, the effector of AI-2 quorum sensing, is vital for the H2O2 stress response in mammary pathogenic Escherichia coli