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News Article

Receptor for Clostridium perfringens beta toxin identified

Clostridium perfringens type C causes severe and lethal necrotic enteritis in newborn piglets

Researchers at the University of Bern have discovered how Clostridium perfringens causes fatal intestinal bleeding in pigs.

Ten years ago, Horst Posthaus’s group in the Institute of Animal Pathology at the University of Bern were able to demonstrate that the beta toxin produced by C. perfringens kills vascular cells, causing bleeding in the intestines. Until now, however, it was unclear why the toxin attacked specifically these cells and not others. Julia Bruggisser, biochemist and doctoral student at the Institute of Animal Pathology, has now succeeded in solving this puzzle in an interdisciplinary collaboration between three faculties. The findings from the study have been published in Cell Host & Microbe.

Around five years ago, lab technician Marianne Wyder from the Institute of Animal Pathology came across a molecule called Platelet-Endothelial Cell Adhesion Molecule-1 (PECAM-1 or CD31). It is located on the surface of various cells and plays a central role in intestinal bleeding in piglets. The CD31 molecule regulates the interaction between inflammatory cells and the blood vessels. It predominantly occurs on cells which are located on the inside of blood vessels (endothelial cells).

During experiments, it was noticed that CD31 and the beta toxin are distributed almost identically on these cells. "Our project resulted from this initial observation," says Horst Posthaus. Julia Bruggisser discovered that the toxin released by the bacteria in the intestine attaches to CD31. Beta toxin is a pore-forming toxin; it perforates the cell membrane and kills the endothelial cells. This results in damage to the vessels and bleeding in the intestine.

The researchers hope that the discovery will lead to the development of better vaccines in order to prevent the fatal disease in pigs. "But we also want to investigate whether the attachment of beta toxin to CD31 on the endothelial cells also allows for the development of new forms of therapy, for vascular disease in humans, for example. We have already started more collaborations within the University of Bern to this end," says Horst Posthaus.

Article: Bruggisser, J., Tarek, B., Wyder, M., Müller, P., von Ballmoos, C., Witz, G., Enzmann, G., Deutsch, U., Engelhardt, B., Posthaus, H. (2020). CD31 (PECAM-1) Serves as the Endothelial Cell-Specific Receptor of Clostridium perfringens β-Toxin. Cell Host & Microbe, online 3 June 2020, doi: 10.1016/j.chom.2020.05.003

Article details

  • Date
  • 05 June 2020
  • Source
  • University of Bern
  • Subject(s)
  • Food Animals