ArticleCell host & microbe2013
Cholera toxin disrupts barrier function by inhibiting exocyst-mediated trafficking of host proteins to intestinal cell junctions.
Article in Cell host & microbe, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 60 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
60 citing papers in PubMed, 103 citations in OpenAlex.
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- New insights into outer membrane vesicles in Gram-negative bacteria from biogenesis to applications.Communications biology · 2026Review
- Distinct Roles of SLC26A3 and CFTR in Surface pH Regulation and Bicarbonate Secretion in Human Intestinal Epithelium.Acta physiologica (Oxford, England) · 2026Article
- Anthrax ET activates Rac1 and RTK signaling to induce F-actin reorganization and endothelial permeability.iScience · 2025Article
- Botulinum neurotoxin Light Chain/A1 uses fast synaptic vesicle cycling to cleave plasma membrane bound SNAP-25.Communications biology · 2025Article
- Genome-Wide Identification Analysis of theGenes · 2025Article
- A new experimental model of peanut allergy in BALB/c and C57BL/6 mice.Frontiers in allergy · 2025Article
- Pushing boundaries: mechanisms enabling bacterial pathogens to spread between cells.Infection and immunity · 2024Review
- Notch Signaling in Insect Development: A Simple Pathway with Diverse Functions.International journal of molecular sciences · 2023Review
- Osteopontin Exacerbates High-Fat Diet-Induced Metabolic Disorders in a Microbiome-Dependent Manner.mBio · 2022Article
- Article
- Enterotoxigenic Escherichia coli heat-labile toxin drives enteropathic changes in small intestinal epithelia.Nature communications · 2022Article
- Inter-Species Rescue of Mutant Phenotype-The Standard for Genetic Analysis of Human Genetic Disorders inInternational journal of molecular sciences · 2022Review
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- Suspected gut barrier disruptors and development of food allergy: Adjuvant effects and early immune responses.Frontiers in allergy · 2022Article
- Cellular Activity ofToxins · 2021Article
- Review
- Endocytosis of Intestinal Tight Junction Proteins: In Time and Space.Inflammatory bowel diseases · 2021Review
- Predicting host dependency factors of pathogens inComputational and structural biotechnology journal · 2021Article
Corrections and comments
- Commented on by
- Erratum issuedCruz-Moreno, Beatriz Cruz [corrected to Cruz-Moreno, Beatriz]
Authors and funding
14 authors at 2 institutions in 2 countries.
Funding
Abstract
Cholera toxin (CT), a virulence factor elaborated by Vibrio cholerae, is sufficient to induce the severe diarrhea characteristic of cholera. The enzymatic moiety of CT (CtxA) increases cAMP synthesis in intestinal epithelial cells, leading to chloride ion (Cl(-)) efflux through the CFTR Cl(-) channel. To preserve electroneutrality and osmotic balance, sodium ions and water also flow into the intestinal lumen via a paracellular route. We find that CtxA-driven cAMP increase also inhibits Rab11/exocyst-mediated trafficking of host proteins including E-cadherin and Notch signaling components to cell-cell junctions in Drosophila, human intestinal epithelial cells, and ligated mouse ileal loops, thereby disrupting barrier function. Additionally, CtxA induces junctional damage, weight loss, and dye leakage in the Drosophila gut, contributing to lethality from live V. cholerae infection, all of which can be rescued by Rab11 overexpression. These barrier-disrupting effects of CtxA may act in parallel with Cl(-) secretion to drive the pathophysiology of cholera.
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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.