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Updated: May 31, 2026
08:00
Enrichment and Detection of Clostridium perfringens Toxinotypes in Retail Food Samples
Published on: October 18, 2019
Interactions between Clostridium perfringens enterotoxin and claudins.
Methods in Molecular Biology (Clifton, N.J.)
|July 1, 2011
Summary
Clostridium perfringens enterotoxin (CPE) causes gastrointestinal illness by forming pores in cells. These pores disrupt cell integrity, leading to cell death and disease.
Area of Science:
- Microbiology
- Cell Biology
- Toxicology
Background:
- Clostridium perfringens enterotoxin (CPE) is linked to food poisoning and antibiotic-associated diarrhea.
- CPE is a 35 kDa polypeptide that initiates disease by binding to cellular receptors.
Purpose of the Study:
- To elucidate the molecular mechanisms of CPE-induced cell damage.
- To characterize the CPE-receptor complexes involved in cellular toxicity.
Main Methods:
- CPE treatment of Caco-2 cells.
- Analysis of CPE-receptor complex formation (CH-1 and CH-2).
- Identification of claudins and occludin within CPE complexes.
Main Results:
- CPE binds claudin receptors, forming a hexameric pore (CH-1) that allows calcium influx.
- CH-1 formation leads to altered cell permeability, cell death (oncosis/apoptosis), and tight junction disruption.
- Claudins -3 and -4 were identified in CH-1 and CH-2 complexes, with claudin-1 also present despite poor binding.
Conclusions:
- CPE induces cell death by forming calcium-permeable pores and disrupting cellular junctions.
- Claudin-3 and -4 are key components of CPE-induced complexes, mediating toxin effects.
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