Related Experiment Video
Updated: Jun 6, 2026

10:41
Detection of Toxin Translocation into the Host Cytosol by Surface Plasmon Resonance
Published on: January 3, 2012
Anthrax toxins--roadblocks for exocytic trafficking.
1Department of Microbiology and Immunology, University of Otago, Dunedin 9054, New Zealand. keith.ireton@otago.ac.nz
Developmental Cell
|November 16, 2010
Summary
Anthrax toxins disrupt vascular function by damaging endothelial cells. Researchers discovered these toxins block the delivery of essential cell junction proteins, impacting the cell barrier.
Area of Science:
- Cell Biology
- Toxicology
- Vascular Biology
Background:
- Anthrax toxins are known to cause vascular dysfunction by compromising the endothelial cell barrier.
- The precise molecular mechanisms underlying this endothelial cell perturbation remain incompletely understood.
Discussion:
- Guichard et al. investigated the molecular mechanisms by which anthrax toxins disrupt endothelial cell junctions.
- The study reveals that anthrax toxins interfere with the exocytic pathway responsible for delivering cadherins to cell-cell junctions.
Key Insights:
- Anthrax toxins antagonize the exocyst complex, a key regulator of exocytosis.
- This antagonism prevents the proper delivery and localization of cadherins, crucial for endothelial cell adhesion and barrier integrity.
- The findings elucidate a novel mechanism of anthrax toxin-induced vascular damage.
Outlook:
- Further research could explore therapeutic strategies targeting the exocyst complex to counteract anthrax toxin effects.
- Understanding this interaction may inform treatments for other conditions involving endothelial barrier dysfunction.
Related Concept Videos
Inhalation Anthrax
Anthrax is a zoonotic disease caused by Bacillus anthracis, a Gram-positive, spore-forming bacterium. It primarily affects herbivorous animals but can be transmitted to humans through skin contact, ingestion, or inhalation of spores.Cutaneous anthrax, the most common form, typically results from direct contact with bacterial spores through skin abrasions and is generally less severe. Gastrointestinal anthrax results from eating undercooked or contaminated meat. It affects the mouth, throat, or...
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...
Receptor-mediated Endocytosis
Receptor-mediated endocytosis is when bulk amounts of specific molecules are imported into a cell after binding to cell surface receptors. The molecules bound to these receptors are taken into the cell through inward folding of the cell surface membrane, which is eventually pinched off into a vesicle within the cell. Structural proteins, such as clathrin, coat the budding vesicle.
Clathrin-Mediated Endocytosis of LDL
One well-characterized example of receptor-mediated endocytosis is the...
Clathrin-Mediated Endocytosis of LDL
One well-characterized example of receptor-mediated endocytosis is the...
Receptor-mediated Endocytosis
Overview
Botulism
Botulism is a life-threatening neuroparalytic condition caused by botulinum neurotoxin, which is produced by the bacterium Clostridium botulinum, a Gram-positive, spore-forming, obligate anaerobe.In adults, the toxin enters the body in different ways: in foodborne botulism, the preformed toxin is absorbed in the intestine. In wound botulism, spores grow in injured tissue and release the toxin into the blood. Infant botulism differs mechanistically from adult forms. In infants, botulism commonly...
Fusion of Secretory Vesicles with the Plasma Membrane
Proteins and neurotransmitters in secretory vesicles can be released from a cell upon vesicle docking, priming, and fusion with the plasma membrane. Vesicles are docked and primed in preparation for the quick exocytosis of their contents in response to a stimulus. The fusion process is mainly carried out by a SNAP Receptor or SNARE complex, consisting of synaptobrevin, syntaxin-1, and SNAP-25.
In 1993, Jim Rothman proposed that the antiparallel pairing of vesicular and transmembrane SNAREs, or...
In 1993, Jim Rothman proposed that the antiparallel pairing of vesicular and transmembrane SNAREs, or...
