Transcriptional Regulator YqeI, Locating at ETT2 Locus, Affects the Pathogenicity of Avian Pathogenic Escherichia coli

SIMPLE SUMMARY: Avian pathogenic Escherichia coli (APEC) is the causative agent of colibacillosis, threatening the development of the poultry industry. The study on APEC’s pathogenic mechanism is of great importance. In this study, we investigated the role of YqeI, a transcriptional regulator locating at E. coli type three secretion system 2 in APEC. The transcriptional results revealed that YqeI affected the expression of the genes involving in bacterial localization, locomotion and biological adhesion. A series experiments also demonstrated that the absence of yqeI decreased the bacterial flagella formation ability, motility ability, antiserum bactericidal ability, adhesion ability and colonization ability. Our data suggested that the transcriptional regulator YqeI indeed participates in the pathogenicity of APEC. ABSTRACT: Avian pathogenic Escherichia coli (APEC) is the leading cause of systemic infections in poultry worldwide and has a hidden threat to public health. Escherichia coli type three secretion system 2 (ETT2), similar to the Salmonella pathogenicity island SPI1, is widely distributed in APEC and associated with virulence. The function of YqeI, which is one of the hypothetical transcriptional regulators locating at the ETT2 locus of APEC, is unknown. In this study, we successfully obtained the mutant strain AE81ΔyqeI of the wild type strain AE81 and performed the transcriptional profiling assays. Additionally, the transcriptional sequencing results revealed that YqeI influenced localization, locomotion and biological adhesion and so on. The transmission electron microscope observation showed that the wild type strain AE81 possessed long curved flagella, whereas the mutant strain AE81ΔyqeI hardly had any. The strain AE81ΔyqeI exhibited lower motility than AE81 after culturing the dilute bacterial suspension on a semisolid medium. It was also found that the survival ability of AE81ΔyqeI weakened significantly when AE81ΔyqeI was cultured with 0%, 10%, 20%, 30%, 40% and 50% SPF serum in PBS, and AE81ΔyqeI had decreased adherence to DF-1 cells compared with AE81 in the bacterial adhesion assay. The bacterial colonization assay indicated that the virulence of AE81ΔyqeI was reduced in the heart, liver, spleen, and lung. These results confirmed that the transcription regulator YqeI is involved in APEC’s pathogenicity, and this study provides clues for future research.