ArticleNature communications2022
Enterotoxigenic Escherichia coli heat-labile toxin drives enteropathic changes in small intestinal epithelia.
Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
34 citing papers in PubMed, 51 citations in OpenAlex.
- Attenuating ETEC virulence using a heat-labile enterotoxin-blocking binding protein.Gut microbes · 2026Article
- Proteomic and functional profiling of suspended jejunal enteroids reveals pharmacokinetic fidelity to native intestine.iScience · 2026Article
- BEST4⁺ cells: a potential hub of intestinal ion transport and diarrhea manipulation.Advanced biotechnology · 2026Review
- Chemical characterization of aconite polysaccharide and its ameliorative effect on ulcerative colitis by regulating gut microbiota and THDCA-driven TGR5/cAMP/PKA/NLRP3 pathway.Journal of pharmaceutical analysis · 2026Article
- Dynamic interaction between Escherichia coli enterotoxins and bacteriocins.The FEBS journal · 2026Article
- The role of the gut microbiota in radiation enteritis: from mechanistic insights to therapeutic applications.Communications biology · 2026Review
- Effect of Limosilactobacillus reuteri SBC5-3 Cell-free Supernatant on Growth Performance, Intestinal Inflammation, and Microbiota in Weaned Piglets Challenged With Enterotoxigenic Escherichia coli K88.Probiotics and antimicrobial proteins · 2026Article
- Evaluating the Immunogenicity of a RecombinantBiology · 2026Article
- De novo nucleotide biosynthesis and its dynamic regulation are crucial for systemic infection by extraintestinal Escherichia coli.PLoS pathogens · 2026Article
- Diverse enteric bacterial, viral, and parasitic pathogen genes are shed in animal feces in Indiana.PloS one · 2026Article
- Article
- An Asset for Food Safety: The Knowledge Behind the Physiological Alterations Induced by ETEC Enterotoxins.Foods (Basel, Switzerland) · 2025Review
- Iron Stress Reprograms Enterocyte Metabolism.Metabolites · 2025Article
- Intestinal inflammation induced by heat-labile toxin-producing enterotoxigenic E: Coli infection and impact on immune responses in an experimental human challenge model.PLoS neglected tropical diseases · 2025Article
- Building a Broader Understanding of EnterotoxigenicOpen forum infectious diseases · 2025Article
- Enhancing phage therapy by coating single bacteriophage-infected bacteria with polymer to preserve phage vitality.Nature biomedical engineering · 2025Article
- Parenteral vaccination with recombinant EtpA glycoprotein impairs enterotoxigenicInfection and immunity · 2025Article
- Prevalence, Molecular Characterization, and Antimicrobial Resistance Profile of EnterotoxigenicFoods (Basel, Switzerland) · 2025Article
- Conserved antigens for enteric vaccines.Vaccine · 2025Review
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
15 authors at 3 institutions in 1 country.
Funding
Abstract
Enterotoxigenic E. coli (ETEC) produce heat-labile (LT) and/or heat-stable (ST) enterotoxins, and commonly cause diarrhea in resource-poor regions. ETEC have been linked repeatedly to sequelae in children including enteropathy, malnutrition, and growth impairment. Although cellular actions of ETEC enterotoxins leading to diarrhea are well-established, their contributions to sequelae remain unclear. LT increases cellular cAMP to activate protein kinase A (PKA) that phosphorylates ion channels driving intestinal export of salt and water resulting in diarrhea. As PKA also modulates transcription of many genes, we interrogated transcriptional profiles of LT-treated intestinal epithelia. Here we show that LT significantly alters intestinal epithelial gene expression directing biogenesis of the brush border, the major site for nutrient absorption, suppresses transcription factors HNF4 and SMAD4 critical to enterocyte differentiation, and profoundly disrupts microvillus architecture and essential nutrient transport. In addition, ETEC-challenged neonatal mice exhibit substantial brush border derangement that is prevented by maternal vaccination with LT. Finally, mice repeatedly challenged with toxigenic ETEC exhibit impaired growth recapitulating the multiplicative impact of recurring ETEC infections in children. These findings highlight impacts of ETEC enterotoxins beyond acute diarrheal illness and may inform approaches to prevent major sequelae of these common infections including malnutrition that impact millions of children.
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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.