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Updated: Dec 15, 2025

Enrichment and Detection of Clostridium perfringens Toxinotypes in Retail Food Samples
Published on: October 18, 2019
Everything Illuminated-Clostridium perfringens β-toxin
1Boston Children's Hospital, Boston, MA 02115, USA; Harvard Medical School, Boston, MA 02115, USA; Harvard Digestive Disease Center, Boston, MA 02115, USA.
Clostridium perfringens β-toxin (CPB) binds to platelet endothelial cell adhesion molecule-1 (PECAM-1) on cells. This interaction forms membrane pores, explaining CPB
Area of Science:
- Microbiology
- Immunology
- Cell Biology
Background:
- Clostridium perfringens beta-toxin (CPB) is a virulence factor implicated in various diseases.
- The specific cellular targets and mechanisms of CPB-induced pathology remain incompletely understood.
Purpose of the Study:
- To elucidate the molecular interactions underlying CPB-mediated cell damage.
- To identify the specific host cell receptor for CPB.
Main Methods:
- In vitro binding assays using purified CPB and various cell lines.
- Microscopy techniques to visualize pore formation.
- Genetic manipulation of cell surface molecules.
Main Results:
- CPB specifically binds to platelet endothelial cell adhesion molecule-1 (PECAM-1), also known as CD31.
- Binding of CPB to PECAM-1 induces the formation of membrane pores.
- Pore formation is dependent on the presence of PECAM-1 on the target cell.
Conclusions:
- PECAM-1 is the primary receptor for Clostridium perfringens beta-toxin.
- The interaction between CPB and PECAM-1 is a key mechanism driving CPB-induced cytotoxicity and disease pathogenesis.
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