Abstract

Polymorphonuclear leukocytes (PMNs) release large quantities of reactive oxygen species (ROS) to kill pathogens. Escherichia coli (E. coli) strains containing a Yersinia high-pathogenicity island (HPI) display increased virulence that is attributable to increased iron scavenging activity, which enhances bacterial growth and limits the availability of iron for use by innate immune cells. ROS generation requires the catalysis of iron. The irp2 gene has been confirmed to be the main gene involved in the synthesis of HPI. In the present study, the effect of pathogenic HPI-positive Yunnandominant (O152) E. coli strains on the respiratory oxidative stress response from PMNs in Yunnan Saba pigs were not explored. The results showed that E. coli containing the HPI can reduce ROS generation by competitively consuming iron in the surrounding environment, while inducing high levels of antioxidases in PMNs. We discovered a novel mechanism by which the HPI protects E.coli from ROS and enhances its virulence in PMNs. These results increase our understanding of the interaction between pathogenic E. coli and host PMNs in Saba pigs.

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