Oxidative stress response in avian pathogenic Escherichia coli.

Abstract

Avian pathogenic Escherichia coli (APEC) leads to significant economic losses in the poultry industry worldwide and restricts the development of the poultry industry. Oxidative stress, through the production of reactive oxygen species (ROS), damage iron‑sulfur (FeS) clusters, cysteine and methionine protein residues, and DNA, and then result in bacterial cells death. APEC has evolved a series of regulation systems to sense and quickly and appropriately respond to oxidative stress. Quorum sensing (QS), second messenger (SM), transcription factors (TFs), small regulatory RNAs (sRNAs), and two-component system (TCS) are important regulation systems ubiquitous in bacteria. It is of great significance to control APEC infection through investigating the molecular regulation mechanism on APEC adapting to oxidative stress. However, how the cross-talk among these regulation systems co-regulates transcription of oxidative stress-response genes in APEC has not been reported. This review suggests exploring connector proteins that co-regulate these regulation systems that co-activate transcription of oxidative stress-response genes to disrupt bacterial antioxidative defense mechanism in APEC, and then using these connector proteins as drug targets to control APEC infection. This review might contribute to illustrating the functional mechanism of APEC adapting to oxidative stress and exploring potential drug targets for the prevention and treatment of APEC infection.