ArticleInfection and immunity2014
Enteropathogenic Escherichia coli inhibits type I interferon- and RNase L-mediated host defense to disrupt intestinal epithelial cell barrier function.
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 22 papers.
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Who cites it
22 citing papers in PubMed, 38 citations in OpenAlex.
- Article
- Gastrointestinal insufficiency is a risk factor for severely burned patients: a case-control study among 185 victims in Kunshan explosion.BMC gastroenterology · 2025Article
- The link between gut microbiota and multiple sclerosis from the perspective of barrier function.Frontiers in immunology · 2025Review
- Type III Secretion System in Intestinal Pathogens and Metabolic Diseases.Journal of diabetes research · 2024Review
- Antimicrobial and Immunomodulatory Potential of Cow Colostrum Extracellular Vesicles (ColosEVs) in an Intestinal In Vitro Model.Biomedicines · 2022Article
- Heat stress inhibits TLR4-NF-κB and TLR4-TBK1 signaling pathways in broilers infected with Salmonella Typhimurium.International journal of biometeorology · 2021Article
- Targeting the gut to treat multiple sclerosis.The Journal of clinical investigation · 2021Review
- Review
- Interferons: Tug of War Between Bacteria and Their Host.Frontiers in cellular and infection microbiology · 2021Review
- New advances in our understanding of the "unique" RNase L in host pathogen interaction and immune signaling.Cytokine · 2020Review
- Intestinal barrier dysfunction in severe burn injury.Burns & trauma · 2019Review
- Intestinal cell migration damage induced by enteropathogenic Escherichia coli strains.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2018Article
- The intestinal barrier in multiple sclerosis: implications for pathophysiology and therapeutics.Brain : a journal of neurology · 2018Review
- Type I and III Interferon in the Gut: Tight Balance between Host Protection and Immunopathology.Frontiers in immunology · 2017Review
- Citrobacter rodentium NleB Protein Inhibits Tumor Necrosis Factor (TNF) Receptor-associated Factor 3 (TRAF3) Ubiquitination to Reduce Host Type I Interferon Production.The Journal of biological chemistry · 2016Article
- The Roles of Type I Interferon in Bacterial Infection.Cell host & microbe · 2016Review
- The Roles of RNase-L in Antimicrobial Immunity and the Cytoskeleton-Associated Innate Response.International journal of molecular sciences · 2016Review
- Encyclopedia of bacterial gene circuits whose presence or absence correlate with pathogenicity--a large-scale system analysis of decoded bacterial genomes.BMC genomics · 2015Article
- MicroRNA-146a constrains multiple parameters of intestinal immunity and increases susceptibility to DSS colitis.Oncotarget · 2015Article
- Salmonella Typhimurium Co-Opts the Host Type I IFN System To Restrict Macrophage Innate Immune Transcriptional Responses Selectively.Journal of immunology (Baltimore, Md. : 1950) · 2015Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Enteropathogenic Escherichia coli (EPEC) primarily infects children in developing countries and causes diarrhea that can be deadly. EPEC pathogenesis occurs through type III secretion system (T3SS)-mediated injection of effectors into intestinal epithelial cells (IECs); these effectors alter actin dynamics, modulate the immune response, and disrupt tight junction (TJ) integrity. The resulting compromised barrier function and increased gastrointestinal (GI) permeability may be responsible for the clinical symptoms of infection. Type I interferon (IFN) mediates anti-inflammatory activities and serves essential functions in intestinal immunity and homeostasis; however, its role in the immune response to enteric pathogens, such as EPEC, and its impact on IEC barrier function have not been examined. Here, we report that IFN-β is induced following EPEC infection and regulates IEC TJ proteins to maintain barrier function. The EPEC T3SS effector NleD counteracts this protective activity by inhibiting IFN-β induction and enhancing tumor necrosis factor alpha to promote barrier disruption. The endoribonuclease RNase L is a key mediator of IFN induction and action that promotes TJ protein expression and IEC barrier integrity. EPEC infection inhibits RNase L in a T3SS-dependent manner, providing a mechanism by which EPEC evades IFN-induced antibacterial activities. This work identifies novel roles for IFN-β and RNase L in IEC barrier functions that are targeted by EPEC effectors to escape host defense mechanisms and promote virulence. The IFN-RNase L axis thus represents a potential therapeutic target for enteric infections and GI diseases involving compromised barrier function.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.