Clostridium difficile is a dangerous intestinal bacterium that can cause severe diarrhoea and life-threatening intestinal infections after long-term treatment with antibiotics. The pharmacologists and toxicologists Professor Dr. Klaus Aktories and Dr. Panagiotis Papatheodorou from the University of Freiburg in Germany have identified the molecular docking site that is responsible for the C. difficile toxin's being able to bind to its receptor on the membrane of the intestinal epithelium. This docking site functions like an elevator, transporting the toxins into the cell's interior. By binding to the surface receptor, the toxins are able to overcome the cell membrane. Once inside the cell, C. difficile exerts its full lethal effect. "Bacteria are becoming increasingly resistant to antibiotics. That's why new types of therapy that aren't based primarily on bacteria are necessary," Dr. Aktories said. "Our goal in the future should be to reduce the toxicological potential of toxins as well," he added. The team of researchers published its results in the May 29, 2015 issue of the Journal of Biological Chemistry. The JBC article is titled “Interaction of the Clostridium difficile Binary Toxin CDT and Its Host Cell Receptor, Lipolysis-Stimulated Lipoprotein Receptor (LSR).” The intestinal pathogen C. difficile is most commonly found in hospitals and is often acquired by older people and people with weakened immune systems. In Western countries, infections with so-called hypervirulent strains of C. difficile are rapidly increasing and are much more dangerous and more difficult to treat. The pathology of C. difficile infections is primarily triggered by two toxins released by the pathogen, which then damage the intestinal epithelium. Particularly dangerous hypervirulent strains produce a third toxin, C. difficile transferase (CDT).
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