ArticleInfection and immunity2014
The type III secretion effector NleF of enteropathogenic Escherichia coli activates NF-κB early during infection.
Article in Infection and immunity, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed.
- The Edwardsiella T3SS effector EseJ enhances NF-κB signaling by stabilizing p65 and promoting TAK1 phosphorylation.PLoS pathogens · 2026Article
- EnteropathogeniceLife · 2026Article
- Attaching and effacing pathogens modulate host mitochondrial structure and function.International review of cell and molecular biology · 2023Review
- Role of UPRFrontiers in cellular and infection microbiology · 2023Review
- Hybrid Vigor: Importance of Hybrid λ Phages in Early Insights in Molecular Biology.Microbiology and molecular biology reviews : MMBR · 2022Review
- Vaccinia virus BTB-Kelch proteins C2 and F3 inhibit NF-κB activation.The Journal of general virology · 2022Article
- Article
- NF-κB Regulation by Gut Microbiota Decides Homeostasis or Disease Outcome During Ageing.Frontiers in cell and developmental biology · 2022Review
- Different effects of cortisol on pro-inflammatory gene expressions in LPS-, heat-killed E.coli-, or live E.coli-stimulated bovine endometrial epithelial cells.BMC veterinary research · 2020Article
- The NF-κB Signaling Pathway, the Microbiota, and Gastrointestinal Tumorigenesis: Recent Advances.Frontiers in immunology · 2020Review
- Vaccinia Virus BBK E3 Ligase Adaptor A55 Targets Importin-Dependent NF-κB Activation and Inhibits CD8Journal of virology · 2019Article
- Clever Cooperation: Interactions Between EspF and Host Proteins.Frontiers in microbiology · 2018Review
- Attaching and effacing (A/E) lesion formation by enteropathogenic E. coli on human intestinal mucosa is dependent on non-LEE effectors.PLoS pathogens · 2017Article
- Bacterial virulence factor inhibits caspase-4/11 activation in intestinal epithelial cells.Mucosal immunology · 2017Article
- Distinct Roles of the Antiapoptotic Effectors NleB and NleF from Enteropathogenic Escherichia coli.Infection and immunity · 2017Article
- Type III Secretion in the Melioidosis PathogenFrontiers in cellular and infection microbiology · 2017Review
- Tir Triggers Expression of CXCL1 in Enterocytes and Neutrophil Recruitment during Citrobacter rodentium Infection.Infection and immunity · 2015Article
- Modulation of the host innate immune and inflammatory response by translocated bacterial proteins.Cellular microbiology · 2015Review
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Authors and funding
5 authors.
Funding
Abstract
The enteric pathogens enteropathogenic Escherichia coli (EPEC) and enterohemorrhagic E. coli employ a type 3 secretion system (T3SS) to manipulate the host inflammatory response during infection. Previously, it has been reported that EPEC, in a T3SS-dependent manner, induces an early proinflammatory response through activation of NF-κB via extracellular signal-regulated kinases 1 and 2 (ERK1/2) and protein kinase Cζ (PKCζ). However, the activation of NF-κB during infection has not yet been attributed to an effector. At later time points postinfection, NF-κB signaling is inhibited through the translocation of multiple effectors, including NleE and NleC. Here we report that the highly conserved non-LEE (locus of enterocyte effacement)-encoded effector F (NleF) shows both diffuse and mitochondrial localization during ectopic expression. Moreover, NleF induces the nuclear translocation of NF-κB p65 and the expression of interleukin 8 (IL-8) following ectopic expression and during EPEC infection. Furthermore, the proinflammatory activity and localization of NleF were dependent on the C-terminal amino acids LQCG. While the C-terminal domain of NleF has previously been shown to be essential for interaction with caspase-4, caspase-8, and caspase-9, the proinflammatory activity of NleF was independent of interaction with caspase-4, -8, or -9. In conclusion, EPEC, through the T3SS-dependent translocation of NleF, induces a proinflammatory response in an NF-κB-dependent manner in the early stages of infection.
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