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UCSD biologists discover cell's defense mechanism against class of disease-causing bacterial toxins

shown to be important for protecting against this class of bacterial toxin.

Aroian and Huffman further discovered that these two genes, SEK1 and KGB1, controlled two "pathways" of biochemical reactions that are essential in allowing roundworms to survive a 30 minute exposure to a high dose of Cry5B toxin. Roundworms missing either of the two genes were hypersensitive to Cry5B and quickly died after such an exposure to a high dose of toxin or to a low, chronic dose of toxin, the scientists found.

Working with Laurence Abrami and F. Gisou van der Goot of the University of Geneva, the scientists found the same basic responses in hamster kidney cells with and without one of the two genes. These cells were exposed to aerolysin, the pore-forming toxin from Aeromonas hydrophila, an antibiotic-resistant bacterium that causes lesions and illness in humans. The results from this second experiment suggest that the gene and the biochemical pathways it controls are a generalized, natural defense mechanism to pore-forming toxins in mammalian cells as well as in roundworms.

Now that scientists have a basic understanding of the biochemical mechanisms that enable cells to defend themselves against pore-forming toxins, biomedical researchers can begin to develop drugs against the rising tide of antibiotic-resistant strains of Staphylococcus aureus, Streptococcus pneumoniae, and other bacteria that use pore-forming toxins in their arsenals.

"Now that we know how cells defend themselves, we can think about developing therapeutic agents to improve a person's defenses against pathogenic bacteria that use this class of toxins," says Aroian. "You can't fight something you don't understand, but now we are starting to get a very basic understanding of how a major class of virulence factors works. In addition we have now the tools to try to understand this in greater detail."

Funding for the project was provided by grants from the National Science Fo
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Contact: Kim McDonald
kmcdonald@ucsd.edu
858-534-7572
University of California - San Diego
12-Jul-2004


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