Abstract |
Clostridium perfringens β-toxin (CPB) is a highly active β-pore-forming toxin (β-PFT) and the essential virulence factor for fatal, necro-hemorrhagic enteritis in animals and humans. The molecular mechanisms involved in CPB's action on its target, the endothelium of small intestinal vessels, are poorly understood. Here, we identify platelet endothelial cell adhesion molecule-1 (CD31 or PECAM-1) as the specific membrane receptor for CPB on endothelial cells. CD31 expression corresponds with the cell-type specificity of CPB, and it is essential for toxicity in cultured cells and mice. Ectopic CD31 expression renders resistant cells and liposomes susceptible to CPB-induced membrane damage. Moreover, the extracellular Ig6 domain of mouse, human, and porcine CD31 is essential for the interaction with CPB. Hence, our results explain the cell-type specificity of CPB in vitro and in the natural disease caused by C. perfringens type C.
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Authors | Julia Bruggisser, Basma Tarek, Marianne Wyder, Philipp Müller, Christoph von Ballmoos, Guillaume Witz, Gaby Enzmann, Urban Deutsch, Britta Engelhardt, Horst Posthaus |
Journal | Cell host & microbe
(Cell Host Microbe)
Vol. 28
Issue 1
Pg. 69-78.e6
(07 08 2020)
ISSN: 1934-6069 [Electronic] United States |
PMID | 32497498
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Copyright | Copyright © 2020 Elsevier Inc. All rights reserved. |
Chemical References |
- Bacterial Toxins
- CPB protein, Clostridium perfringens
- Platelet Endothelial Cell Adhesion Molecule-1
- Virulence Factors
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Topics |
- Amino Acid Sequence
- Animals
- Bacterial Toxins
(metabolism)
- Cell Line
- Cells, Cultured
- Clostridium Infections
(microbiology)
- Clostridium perfringens
(pathogenicity, physiology)
- Endothelial Cells
(metabolism, microbiology)
- Female
- Humans
- Male
- Mice
- Mice, Inbred C57BL
- Mice, Knockout
- Platelet Endothelial Cell Adhesion Molecule-1
(genetics, metabolism)
- Protein Interaction Domains and Motifs
- Swine
- Virulence Factors
(metabolism)
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