YqeH contributes to avian pathogenic Escherichia coli pathogenicity by regulating motility, biofilm formation, and virulence

Avian pathogenic Escherichia coli (APEC) is a pathotype of extraintestinal pathogenic E. coli and one of the most serious infectious diseases of poultry. It not only causes great economic losses to the poultry industry, but also poses a serious threat to public health worldwide. Here, we examined the role of YqeH, a transcriptional regulator located at E. coli type III secretion system 2 (ETT2), in APEC pathogenesis. To investigate the effects of YqeH on APEC phenotype and virulence, we constructed a yqeH deletion mutant (APEC40-Delta yqeH) and a complemented strain (APEC40-C Delta yqeH) of APEC40. Compared with the wild type (WT), the motility and biofilm formation of APEC40-Delta yqeH were significantly reduced. The yqeH mutant was highly attenuated in a chick infection model compared with WT, and showed severe defects in its adherence to and invasion of chicken embryo fibroblast DF-1 cells. However, the mechanisms underlying these phenomena were unclear. Therefore, we analyzed the transcriptional effects of the yqeH deletion to clarify the regulatory mechanisms of YqeH, and the role of YqeH in APEC virulence. The deletion of yqeH downregulated the transcript levels of several flagellum-, biofilm-, and virulence-related genes. Our results demonstrate that YqeH is involved in APEC pathogenesis, and the reduced virulence of APEC40-Delta yqeH may be related to its reduced motility and biofilm formation.

Automated summary

This study investigates the role of transcriptional regulator YqeH in the pathogenicity of avian pathogenic Escherichia coli (APEC). The results show that the deletion of YqeH leads to reduced motility and biofilm formation, resulting in decreased virulence of APEC. Additionally, YqeH regulates the transcriptional levels of genes associated with flagellum, biofilm, and virulence, impacting the pathogenicity of APEC.