ArticleInfection and immunity2007
Enteropathogenic Escherichia coli-induced epidermal growth factor receptor activation contributes to physiological alterations in intestinal epithelial cells.
Article in Infection and immunity, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
22 citing papers in PubMed, 31 citations in OpenAlex.
- EnterohemorrhagicInfection and immunity · 2024Article
- Alterations in the gut microbiota and their metabolites in human intestinal epithelial cells of patients with colorectal cancer.Molecular biology reports · 2024Article
- Multi-omics analysis reveals the effects of microbiota on oral homeostasis.Frontiers in immunology · 2022Article
- The Four Horsemen in Colon Cancer.Journal of oncology · 2019Review
- Clever Cooperation: Interactions Between EspF and Host Proteins.Frontiers in microbiology · 2018Review
- Modulation of host signaling in the inflammatory response by enteropathogenic Escherichia coli virulence proteins.Cellular & molecular immunology · 2017Review
- Novel Host Proteins and Signaling Pathways in Enteropathogenic E. coli Pathogenesis Identified by Global Phosphoproteome Analysis.Molecular & cellular proteomics : MCP · 2015Article
- Article
- Effects of the Probiotic Enterococcus faecium and Pathogenic Escherichia coli Strains in a Pig and Human Epithelial Intestinal Cell Model.Scientifica · 2015Article
- Enteropathogenic Escherichia coli dynamically regulates EGFR signaling in intestinal epithelial cells.American journal of physiology. Gastrointestinal and liver physiology · 2014Article
- Pathogenesis of human enterovirulent bacteria: lessons from cultured, fully differentiated human colon cancer cell lines.Microbiology and molecular biology reviews : MMBR · 2013Review
- Article
- The enteropathogenic Escherichia coli-secreted protein EspZ inhibits host cell apoptosis.Infection and immunity · 2012Article
- Polyethylene glycol diminishes pathological effects of Citrobacter rodentium infection by blocking bacterial attachment to the colonic epithelia.Gut microbes · 2011Article
- Tumor suppressor FOXO3 mediates signals from the EGF receptor to regulate proliferation of colonic cells.American journal of physiology. Gastrointestinal and liver physiology · 2011Article
- Activation of Akt by the bacterial inositol phosphatase, SopB, is wortmannin insensitive.PloS one · 2011Article
- NleH effectors interact with Bax inhibitor-1 to block apoptosis during enteropathogenic Escherichia coli infection.Proceedings of the National Academy of Sciences of the United States of America · 2010Article
- ERBBs in the gastrointestinal tract: recent progress and new perspectives.Experimental cell research · 2009Review
- Enteropathogenic Escherichia coli subverts phosphatidylinositol 4,5-bisphosphate and phosphatidylinositol 3,4,5-trisphosphate upon epithelial cell infection.Molecular biology of the cell · 2009Article
- Enteropathogenic E. coli-induced barrier function alteration is not a consequence of host cell apoptosis.American journal of physiology. Gastrointestinal and liver physiology · 2008Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The diarrheagenic pathogen enteropathogenic Escherichia coli (EPEC) is responsible for significant infant mortality and morbidity, particularly in developing countries. EPEC pathogenesis relies on a type III secretion system-mediated transfer of virulence effectors into host cells. EPEC modulates host cell survival and inflammation, although the proximal signaling pathways have not been well defined. We therefore examined the effect of EPEC on the epidermal growth factor receptor (EGFR), a known upstream activator of both the prosurvival phosphoinositide 3-kinase/Akt and proinflammatory mitogen-activated protein (MAP) kinase pathways. EPEC induced the autophosphorylation of EGFR in intestinal epithelial cells within 15 min postinfection, with maximal phosphorylation being observed at 4 h. Filter-sterilized supernatants of EPEC cultures also stimulated EGFR phosphorylation, suggesting that a secreted component(s) contributes to this activity. EPEC-induced EGFR phosphorylation was blocked by the pharmacological inhibitor tyrphostin AG1478, as well as by EGFR-neutralizing antibodies. Inhibition of EGFR phosphorylation by AG1478 had no effect on bacterial adherence, actin recruitment to sites of attachment, or EPEC-induced epithelial barrier function alteration. EPEC-mediated Akt phosphorylation, however, was inhibited by both AG1478 and EGFR-neutralizing antibodies. Correspondingly, inhibition of EGFR activation increased the apoptosis/necrosis of infected epithelial cells. Inhibition of EGFR phosphorylation also curtailed EPEC-induced ERK1/2 (MAP kinase) phosphorylation and, correspondingly, the production of the proinflammatory cytokine interleukin-8 by infected epithelial cells. Our studies suggest that EGFR is a key proximal signaling molecule during EPEC pathogenesis.
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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.