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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-Δ yqeH ) and a complemented strain (APEC40-CΔ yqeH ) of APEC40. Compared with the wild type (WT), the motility and biofilm formation of APEC40-Δ 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-Δ yqeH  may be related to its reduced motility and biofilm formation.

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