ArticlePLoS pathogens2017
Epithelial cells detect functional type III secretion system of enteropathogenic Escherichia coli through a novel NF-κB signaling pathway.
Article in PLoS pathogens, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed.
- A Bifunctional T3SS-Effector Simultaneously Cleaves Host MAP Kinase and Inhibits PPM1A Phosphatase.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- The sequence of events of enteropathogeniciScience · 2024Article
- A Bittersweet Kiss of Gram-Negative Bacteria: The Role of ADP-Heptose in the Pathogenesis of Infection.Microorganisms · 2023Review
- Does postcholecystectomy increase the risk of colorectal cancer?Frontiers in microbiology · 2023Review
- The subversion of toll-like receptor signaling by bacterial and viral proteases during the development of infectious diseases.Molecular aspects of medicine · 2022Review
- Whole-genome characterization of hemolytic uremic syndrome-causing Shiga toxin-producingVirulence · 2021Article
- Effects of Pretreatment with Bifidobacterium bifidum Using 16S Ribosomal RNA Gene Sequencing in a Mouse Model of Acute Colitis Induced by Dextran Sulfate Sodium.Medical science monitor : international medical journal of experimental and clinical research · 2021Article
- Shiga toxin remodels the intestinal epithelial transcriptional response to Enterohemorrhagic Escherichia coli.PLoS pathogens · 2021Article
- Clustering of Tir during enteropathogenic E. coli infection triggers calcium influx-dependent pyroptosis in intestinal epithelial cells.PLoS biology · 2020Article
- Article
- The NF-κB Signaling Pathway, the Microbiota, and Gastrointestinal Tumorigenesis: Recent Advances.Frontiers in immunology · 2020Review
- ALPK1: a pattern recognition receptor for bacterial ADP-heptose.Precision clinical medicine · 2018Article
- Article
- Cooperative Immune Suppression by Escherichia coli and Shigella Effector Proteins.Infection and immunity · 2018Review
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Authors and funding
11 authors.
Funding
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Abstract
Enteropathogenic Escherichia coli (EPEC), a common cause of infant diarrhea, is associated with high risk of mortality in developing countries. The primary niche of infecting EPEC is the apical surface of intestinal epithelial cells. EPEC employs a type three secretion system (TTSS) to inject the host cells with dozens of effector proteins, which facilitate attachment to these cells and successful colonization. Here we show that EPEC elicit strong NF-κB activation in infected host cells. Furthermore, the data indicate that active, pore-forming TTSS per se is necessary and sufficient for this NF-κB activation, regardless of any specific effector or protein translocation. Importantly, upon infection with wild type EPEC this NF-κB activation is antagonized by anti-NF-κB effectors, including NleB, NleC and NleE. Accordingly, this NF-κB activation is evident only in cells infected with EPEC mutants deleted of nleB, nleC, and nleE. The TTSS-dependent NF-κB activation involves a unique pathway, which is independent of TLRs and Nod1/2 and converges with other pathways at the level of TAK1 activation. Taken together, our results imply that epithelial cells have the capacity to sense the EPEC TTSS and activate NF-κB in response. Notably, EPEC antagonizes this capacity by delivering anti-NF-κB effectors into the infected cells.
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