Many proteins secreted by pathogenic bacteria are toxins that act on specific target cells in the body of the host. To develop novel therapies, it is crucial to understand the mechanisms underlying the targeted attack exerted by these powerful bacterial weapons.
Pathogenic clostridia, such as C. perfringens, C. botulinum, C. chauvoei, C. septicum, etc., cause severe diseases in animals and humans. The pathogenesis of many of these diseases is poorly understood. Clostridia produce a wide range of exotoxins to manipulate their hosts. Amongst these toxins are some of the most potent bacterial exotoxins known, such as botulinum or tetanus toxin.
We currently focus on the cellular and molecular effects of Clostridium perfringens beta-toxin on target cells. The toxin is known as the essential virulence factor of C. perfringens type C strains, which cause a fatal acute necrotizing enteritis in pigs and other hosts, including humans. The toxin belongs to the family of hemolysin-beta-pore-forming toxins and forms small pores in the membrane of target cells. This leads to cell death and the associated lesions in affected organs.
We previously identified endothelial cells as primary targets for this toxin and established cell culture based in vitro models to investigate the molecular mechanisms of beta-toxin induced endothelial damage. Besides this, we perform studies on the control of C. perfringens type C in Swiss pig herds. Our research has been funded by the Swiss National Science Foundation (SNF) and the Federal Food Safety and Veterinary Office (FSVO).
Besides our primary research topic we offer support for research groups at our faculty and outside as part of our COMPATH platform.