Nanotechnology boosts war on superbugs
During the study Dr McKendry, Joseph Ndieyira, Moyu Watari and coworkers used cantilever arrays – tiny levers no wider than a human hair – to examine the process which ordinarily takes place in the body when vancomycin binds itself to the surface of the bacteria. They coated the cantilever array with mucopeptides from bacterial cell walls and found that as the antibiotic attaches itself, it generates a surface stress on the bacteria which can be detected by a tiny bending of the levers. The team suggests that this stress contributes to the disruption of the cell walls and the breakdown of the bacteria.
The interdisciplinary team went on to compare how vancomycin interacts with both non-resistant and resistant strains of bacteria. The 'superbugs' are resistant to antibiotics because of a simple mutation which deletes a single hydrogen bond from the structure of their cell walls. This small change makes it approximately 1,000 times harder for the antibiotic to attach itself to the bug, leaving it much less able to disrupt the cells' structure, and therefore therapeutically ineffective.
"The cell wall of these bugs is weakened by the antibiotic, ultimately killing the bacteria," said Dr McKendry. "Our research on cantilever sensors suggests that the cell wall is disrupted by a combination of local antibiotic-mucopeptide binding and the spatial mechanical connectivity of these events. Investigating both these binding and mechanical influences on the cells' structure could lead to the development of more powerful and effective antibiotics in future."
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