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

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.

Avian Pathogenic Escherichia coli (APEC): An Overview of Virulence and Pathogenesis Factors, Zoonotic Potential, and Control Strategies

“…Among the different bacterial secretion systems, two secretion systems (type III and VI) contribute to APEC pathogenesis [ 11 , 12 ]. The regulators (EtrA and YqeI) [ 12 , 78 ] and ATPase (EivC) [ 79 ] of the type III secretion system 2 (ETT2) play a role in motility, adhesion, intracellular survival, proliferation, colonization, resistance to phagocytosis and serum bactericidal activity, expression of fimbriae genes, and the downregulation of pro-inflammatory cytokine responses. Similarly, different components of type VI secretion system, DotU (organelle trafficking protein), IcmF (intracellular multiplication factor), Hcp (hemolysis co-regulation protein), CpxR, CpxA (envelope stress response system), ClpV (ATPase), and VrgG (secreted protein) mediate interbacterial competition, adhesion, invasion, intracellular survival, colonization, motility, biofilm formation, production of type 1 fimbriae, resistance to serum bactericidal activity, and modulation of intracellular host responses (IL-8, IL-1β) [ 11 , 40 , 80 , 81 , 82 , 83 , 84 , 85 ].…”

Transcription Regulator YgeK Affects the Virulence of Avian Pathogenic Escherichia coli

“…Flagella are more locomotive organelles in E. coli, and critical for biofilm formation and bacterial virulence [24,25]. Several studies revealed that transcriptional regulators YqeI and ATPase EivC both influence APEC's flagella and motility [20,21], and this study supplements another transcriptional regulator in the ETT2 cluster that has an effect on APEC's flagella and motility. Serum resistance is a prerequisite for septicemia, which is a typical symptom of avian colibacillosis [26].…”

“…The sequence of the ETT2 cluster and YgeK in AE81 was obtained from whole-genome sequencing [ 21 ]. The whole-genome sequencing library was prepared by Novogene Co., Ltd.…”

“…After culturing overnight, bacteria were washed with PBS three times and concentrated (OD 600 = 2.0). The concentrated bacteria were dripped on a 0.25% semisolid medium and incubated for 8 h at 37 • C. Motility was assessed by examining the radius of the bacterial migration of the plate [21].…”

“…The intact ETT2 locus is 29.9 kb with 35 genes, including yqe (ecs3703–3706), yge (ecs3707–3712), epr (ecs3716–3719), etr (ecs3720), epa (ecs3721–3726), and eiv (ecs3727–3737) [ 18 ]; however, not all 35 genes exist in clinical E. coli isolates. Though the presence of ETT2 is often accompanied by extensive deletions and insertions in clinical E. coli isolates, some studies showed that the ETT2 cluster or the genes within the cluster were vital for virulence in ExPEC strains, such as the ETT2 cluster in UPEC, ETT2 ATPase EivC in APEC, and ETT2 transcriptional regulator YqeI in APEC [ 19 , 20 , 21 ].…”