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Effect of Clostridium perfringens β-Toxin on Platelets
Anne Thiel1, Helga Mogel2, Julia Bruggisser3
1Department of Infectious Diseases and Pathobiology, Institute of Animal Pathology, Vetsuisse Faculty, University of Bern, 3012 Bern, Switzerland. anne.thiel@vetsuisse.unibe.ch.
Toxins
|October 25, 2017
Summary
Clostridium perfringens beta-toxin (CPB) targets platelets, impairing their function and causing cell death. This finding reveals CPB
Area of Science:
- Veterinary Pathology
- Microbiology
- Hematology
Background:
- Clostridium perfringens beta-toxin (CPB) is a key virulence factor in C. perfringens type C infections.
- CPB causes hemorrhagic enteritis in animals and humans, with early vascular lesions observed in pigs.
Purpose of the Study:
- To investigate the effect of CPB on platelets and their role in primary hemostasis.
- To determine if CPB directly impacts platelet function.
Main Methods:
- CPB was applied to porcine and human platelets in vitro.
- Platelet aggregation, ultrastructure, and response to thrombin were analyzed.
- Cell viability assays were performed to assess CPB-induced cell death.
Main Results:
- CPB binds to both porcine and human platelets.
- CPB induces time- and dose-dependent platelet cell death and ultrastructural changes.
- Platelet aggregation was significantly reduced, and thrombin-induced activation was inhibited.
Conclusions:
- CPB directly affects platelet physiology, counteracting primary hemostasis.
- Platelets are identified as a novel target cell for CPB.
- This expands the understanding of CPB's role in C. perfringens type C enteritis pathogenesis.
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