ArticleFrontiers in microbiology2014
DotU expression is highly induced during in vivo infection and responsible for virulence and Hcp1 secretion in avian pathogenic Escherichia coli.
Article in Frontiers in microbiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 41 citations in OpenAlex.
- Genomic characterization of the type VI secretion system in extraintestinal pathogenicMicrobiology spectrum · 2026Article
- Quorum-sensing regulator LsrR modulates avian pathogenicInfection and immunity · 2026Article
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- Molecular Characterization and Antibiotic Resistance of Avian PathogenicAnimals : an open access journal from MDPI · 2025Article
- TssL2 of T6SS2 is required for mobility, biofilm formation, wrinkly phenotype formation, and virulence of Vibrio parahaemolyticus SH112.Applied microbiology and biotechnology · 2024Article
- TheVaccines · 2024Article
- Hcp Proteins of the Type VI Secretion System Promote Avian PathogenicLife (Basel, Switzerland) · 2022Article
- Isolation, Molecular Characterization, and Antibiotic Resistance of Avian PathogenicVeterinary sciences · 2022Article
- Avian PathogenicPathogens (Basel, Switzerland) · 2021Review
- Article
- The Ferric Uptake Regulator Represses Type VI Secretion System Function by Binding Directly to theInfection and immunity · 2019Article
- The CpxR regulates type VI secretion system 2 expression and facilitates the interbacterial competition activity and virulence of avian pathogenic Escherichia coli.Veterinary research · 2019Article
- Acetate metabolic requirement of avian pathogenic Escherichia coli promotes its intracellular proliferation within macrophage.Veterinary research · 2019Article
- Type VI Secretion System in PathogenicFrontiers in microbiology · 2019Review
- A Novel PhoP/PhoQ Regulation Pathway Modulates the Survival of Extraintestinal PathogenicFrontiers in immunology · 2018Article
- Escherichia coli type III secretion system 2 (ETT2) is widely distributed in avian pathogenic Escherichia coli isolates from Eastern China.Epidemiology and infection · 2016Article
- The Type VI Secretion System in Escherichia coli and Related Species.EcoSal Plus · 2016Review
- AutA and AutR, Two Novel Global Transcriptional Regulators, Facilitate Avian Pathogenic Escherichia coli Infection.Scientific reports · 2016Article
- A Panel of Stably Expressed Reference Genes for Real-Time qPCR Gene Expression Studies of Mallards (Anas platyrhynchos).PloS one · 2016Article
- Escherichia coli Type III Secretion System 2 ATPase EivC Is Involved in the Motility and Virulence of Avian Pathogenic Escherichia coli.Frontiers in microbiology · 2016Article
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9 authors at 3 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Type VI secretion systems (T6SSs) contribute to pathogenicity in many pathogenic bacteria. Three distinguishable T6SS loci have been discovered in avian pathogenic Escherichia coli (APEC). The sequence of APEC T6SS2 locus is highly similar to the sequence of the newborn meningitis Escherichia coli (NMEC) RS218 T6SS locus, which might contribute to meningitis pathogenesis. However, little is known about the function of APEC T6SS2. We showed that the APEC T6SS2 component organelle trafficking protein (DotU) could elicit antibodies in infected ducks, suggesting that DotU might be involved in APEC pathogenicity. To investigate DotU in APEC pathogenesis, mutant and complemented strains were constructed and characterized. Inactivation of the APEC dotU gene attenuated virulence in ducks, diminished resistance to normal duck serum, and reduced survival in macrophage cells and ducks. Furthermore, deletion of the dotU gene abolished hemolysin-coregulated protein (Hcp) 1 secretion, leading to decreased interleukin (IL)-6 and IL-8 gene expression in HD-11 chicken macrophages. These functions were restored for the complementation strain. Our results demonstrated that DotU plays key roles in the APEC pathogenesis, Hcp1 secretion, and intracellular host response modulation.
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