Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Cholera01:25

Cholera

Cholera is an acute gastrointestinal disease caused by the Gram-negative bacterium Vibrio cholerae. It is transmitted primarily via the fecal-oral route through the ingestion of contaminated water or food.Vibrio cholerae is a motile, Gram-negative bacterium of the family Vibrionaceae, primarily associated with waterborne outbreaks in areas with inadequate sanitation. Although over 200 serogroups of V. cholerae exist, only O1 and O139 are responsible for epidemic cholera. The O1 serogroup,...
Tight Junctions01:29

Tight Junctions

Tight junctions are molecular seals between cells that prevent the leaking of fluids, ions, and other small solutes across cavities and compartments in multicellular organisms. They are mainly composed of claudin and occludin transmembrane proteins, and other proteins such as tricellulin and JAM (junctional adhesion molecule). All these proteins are 4-pass transmembrane proteins, except JAM, which is a single-pass transmembrane protein belonging to the immunoglobulin superfamily. The...
Notch Signaling Pathway03:14

Notch Signaling Pathway

The Notch signaling pathway is a major intracellular signaling pathway that is highly conserved over a broad spectrum of metazoan species. It stands unique from other intracellular signaling mechanisms in animals because notch protein itself acts as the receptor as well as the primary signaling molecule.
The Notch gene came into the limelight in 1914 after the discovery that its mutation in Drosophila melanogaster leads to a serrated (or "notched") wing margin phenotype. It was not until 1985...
Notch Signaling Pathway03:14

Notch Signaling Pathway

The Notch signaling pathway is a major intracellular signaling pathway that is highly conserved over a broad spectrum of metazoan species. It stands unique from other intracellular signaling mechanisms in animals because notch protein itself acts as the receptor as well as the primary signaling molecule.
The Notch gene came into the limelight in 1914 after the discovery that its mutation in Drosophila melanogaster leads to a serrated (or "notched") wing margin phenotype. It was not until 1985...
Bacterial Toxins01:12

Bacterial Toxins

Bacterial toxins are sophisticated virulence factors that enable pathogenic bacteria to interact with, invade, and damage host tissues. These toxins fall broadly into two types: protein exotoxins, which are secreted into the environment and target specific host receptors, and lipopolysaccharide endotoxins, which are structural components of the bacterial outer membrane released primarily during bacterial lysis or membrane shedding. Exotoxins generally act more selectively, binding to cell...
Bacterial Gastroenteritis01:18

Bacterial Gastroenteritis

Bacterial gastroenteritis, characterized by diarrhea, abdominal cramps, and vomiting, is often caused by ingestion of contaminated food or water and is frequently associated with pathogenic Escherichia coli strains. These microbes exploit two principal mechanisms to inflict disease.Shiga toxin–producing E. coli, also referred to as STEC—notably O157:H7—release Shiga toxins that target ribosomes, blocking protein synthesis. The B subunit of the toxin binds the host glycolipid receptor...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Infants who develop BPD have an airway endotype defined by vimentin expression and ciliary loss.

American journal of respiratory cell and molecular biology·2026
Same author

UC-associated autoantibodies to αvβ6 inhibit mucosal TGFβ activation and predispose to intestinal inflammation.

bioRxiv : the preprint server for biology·2026
Same author

From Gut to Systemic Circulation: Molecular Strategies of Botulinum Neurotoxin Complexes.

Toxins·2026
Same author

T Cell Autocrine Hyaluronan Forms Complex Structures in CD4 T Cell Cytoplasm and Plays a Critical Role in Formation of the Immune Synapse.

The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society·2025
Same author

Screening of gene function in cell intoxication by CNF1 links Sec61 translocon to Rac1 GTPase activity.

mBio·2025
Same author

Infants who develop BPD have an airway endotype defined by vimentin expression and ciliary loss.

bioRxiv : the preprint server for biology·2025
Same journal

Gut commensal Bacteroides-derived pantothenic acid alleviates metabolic syndrome.

Cell host & microbe·2026
Same journal

Predicting antimicrobial resistance for precision medicine.

Cell host & microbe·2026
Same journal

Meta-analysis reveals microbiome signatures for colorectal cancer that are universal across age groups and sequencing methods.

Cell host & microbe·2026
Same journal

Single-cell detection and quantification of the microbiota by MicFLY.

Cell host & microbe·2026
Same journal

Suppression of host salicylic acid defense by a phloem-colonizing pathogen effector in citrus Huanglongbing.

Cell host & microbe·2026
Same journal

CBASS limits bacteriophage production while maintaining cell viability in Pseudomonas aeruginosa.

Cell host & microbe·2026
See all related articles

Related Experiment Video

Updated: May 7, 2026

Detection of Toxin Translocation into the Host Cytosol by Surface Plasmon Resonance
10:41

Detection of Toxin Translocation into the Host Cytosol by Surface Plasmon Resonance

Published on: January 3, 2012

Cholera toxin notches epithelial junctions.

Emmanuel Lemichez1, Caroline Stefani

  • 1Inserm U1065, Centre Méditerranéen de Médecine Moléculaire, C3M, Université de Nice-Sophia Antipolis, 151 Route St Antoine de Ginestière, BP 2 3194, 06204 Nice Cedex, France.

Cell Host & Microbe
|September 17, 2013
PubMed
Summary
This summary is machine-generated.

Cholera toxin disrupts intestinal barrier function. This toxin affects the delivery of proteins to cell junctions, leading to watery diarrhea during Vibrio cholerae infections.

More Related Videos

Determination of Tolerable Fatty Acids and Cholera Toxin Concentrations Using Human Intestinal Epithelial Cells and BALB/c Mouse Macrophages
09:39

Determination of Tolerable Fatty Acids and Cholera Toxin Concentrations Using Human Intestinal Epithelial Cells and BALB/c Mouse Macrophages

Published on: May 30, 2013

Sensing of Barrier Tissue Disruption with an Organic Electrochemical Transistor
11:17

Sensing of Barrier Tissue Disruption with an Organic Electrochemical Transistor

Published on: February 10, 2014

Related Experiment Videos

Last Updated: May 7, 2026

Detection of Toxin Translocation into the Host Cytosol by Surface Plasmon Resonance
10:41

Detection of Toxin Translocation into the Host Cytosol by Surface Plasmon Resonance

Published on: January 3, 2012

Determination of Tolerable Fatty Acids and Cholera Toxin Concentrations Using Human Intestinal Epithelial Cells and BALB/c Mouse Macrophages
09:39

Determination of Tolerable Fatty Acids and Cholera Toxin Concentrations Using Human Intestinal Epithelial Cells and BALB/c Mouse Macrophages

Published on: May 30, 2013

Sensing of Barrier Tissue Disruption with an Organic Electrochemical Transistor
11:17

Sensing of Barrier Tissue Disruption with an Organic Electrochemical Transistor

Published on: February 10, 2014

Area of Science:

  • Microbiology
  • Cell Biology
  • Gastroenterology

Background:

  • Cholera toxin (CT) from Vibrio cholerae causes severe watery diarrhea.
  • Intestinal barrier integrity is crucial for gut health.

Purpose of the Study:

  • To elucidate the mechanism by which cholera toxin impairs intestinal barrier function.

Main Methods:

  • Investigated the role of cyclic AMP (cAMP) signaling.
  • Examined the involvement of Rab11 and exocyst proteins.
  • Analyzed the delivery of endocytic recycling cargo to cell-cell junctions.

Main Results:

  • CT induces cyclic AMP (cAMP) production.
  • cAMP disrupts the transport of proteins essential for cell-cell junctions.
  • This disruption affects the delivery of endocytic recycling cargo.

Conclusions:

  • Cholera toxin compromises intestinal epithelium barrier function.
  • Disruption of Rab11- and exocyst-dependent pathways is key to CT's effect.
  • Understanding this mechanism offers insights into cholera pathogenesis.