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Avian pathogenic Escherichia coli (APEC) causes a variety of extraintestinal diseases known as colibacillosis and is responsible for significant economic losses in the poultry industry worldwide. Biofilm formation results in increased morbidity and persistent infections, and is the main reason for the difficult treatment of colibacillosis with antimicrobial agents. It is reported that the transcriptional regulator McbR regulates biofilm formation and mucoidy by repressing the expression of the periplasmic protein YbiM, and activates the transcription of the yciGFE operon by binding to the yciG promoter in E. coli K-12. However, whether McbR regulates biofilm formation and H2O2 stress response in APEC has been not reported. The present study showed that, in the clinical isolate APECX40, the deletion of mcbR increased biofilm formation by upregulating the transcription of the biofilm-associated genes bcsA, fliC, wcaF , and fimA. In addition, the deletion of mcbR decreased H2O2 stress response by downregulating the transcript levels of the stress-associated genes yciF and yciE. The electrophoretic mobility shift assays confirmed that McbR directly binds to the promoter regions of yciG and yciF. This study may provide new clues to understanding gene regulation in APEC. [ABSTRACT FROM AUTHOR]

Avian pathogenic Escherichia coli (APEC) causes a variety of extraintestinal diseases known as colibacillosis and is responsible for significant economic losses in the poultry industry worldwide. Biofilm formation results in increased morbidity and persistent infections, and is the main reason for the difficult treatment of colibacillosis with antimicrobial agents. It is reported that the transcriptional regulator McbR regulates biofilm formation and mucoidy by repressing the expression of the periplasmic protein YbiM, and activates the transcription of the yciGFE operon by binding to the yciG promoter in E. coli K-12. However, whether McbR regulates biofilm formation and H2O2 stress response in APEC has been not reported. The present study showed that, in the clinical isolate APECX40, the deletion of mcbR increased biofilm formation by upregulating the transcription of the biofilm-associated genes bcsA, fliC, wcaF, and fimA. In addition, the deletion of mcbR decreased H2O2 stress response by downregulating the transcript levels of the stress-associated genes yciF and yciE. The electrophoretic mobility shift assays confirmed that McbR directly binds to the promoter regions of yciG and yciF. This study may provide new clues to understanding gene regulation in APEC., (© Crown copyright 2019.)