OxyR controls Actinobacillus pleuropneumoniae toxin production and virulence
Actinobacillus pleuropneumoniae is the causative agent of porcine pleuropneumonia, which has a high prevalence and mortality rate and can result in significant economic losses worldwide. The ability of A. pleuropneumoniae to defend itself against reactive oxygen species produced by host effector cells is a prerequisite for its survival. OxyR is a conserved bacterial transcription factor with a key role in oxidative stress response; however, little is known about its biological role in A. pleuropneumoniae. In this study, we demonstrate that the disruption of the oxyR gene reduces urease activity and increases toxin production and catalase expression. The oxyR disruption mutant was less virulent in the mouse model of infection, and the adhesion ability of PK-15 cells was reduced by three-fold.