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The physicists at McMaster University have for the first time identified a simple mechanism used by potentially life-threatening bacteria to fight antibiotics, a discovery that offers new insights into how germs adapt and shape themselves. feature at a level of detail never seen before.
The results, published today in the journal Nature Biology of communication, could have implications in the global fight against antibiotic resistance, allowing the design of more effective and more effective drugs to fight against infections.
"There are many, many bacteria and antibiotics, but by providing a basic model that applies to many of them, we can better understand how to improve and predict resistance," says Professor Maikel Rheinstädter at the Department of Physics and Astronomy McMaster and lead author of the study.
The researchers examined the interaction of bacterial membranes with the antibiotic polymyxin B (PmB), commonly used to treat urinary tract infections, meningitis, blood and eye infections.
They focused on PMB because it was once considered the most powerful drug of its kind, a last line of defense for doctors when nothing else worked. This status was questioned in 2016 when Chinese scientists discovered a gene that allowed bacteria to become resistant even to polymyxins.
"We wanted to know how this particular bacterium was stopping this drug in this particular case," said Adree Khondker, undergraduate student in health sciences and first author of the study. "If we can understand that, we can design better antibiotics."
Using techniques commonly used by physicists for materials research, the team used highly specialized equipment to scan the bacterial membrane, capturing images with such fine resolution that they could visualize individual molecules. at about 1 / 1,000,000 of the width of a human hair. .
"If you take the bacterial cell and add this medicine, holes will form in the wall, acting like a puncher and killing the cell, but there has been a lot of debate about how these holes were formed." explains Khondker.
Researchers know that the basic laws of physics apply when these antibiotics work properly: because the drug is positively charged, it is attracted to negatively charged bacteria. At the same time, the bacterial membrane uses a repulsive force to try to repel the drug.
With the help of images and simulations, researchers have identified the part of the antibiotic that enters the membrane, where it enters and how deep it enters. They simulated these processes on microsecond time scales with high end gaming computers in their lab.
They determined that when a bacterium became resistant, its membrane is stiffer and the load is lower, which makes it much less attractive to the drug and more difficult to penetrate. "For drugs, it's like cutting Jello to cut through the rock." Khondker says.
"There has been a lot of speculation about this mechanism," said Rheinstädter. "But for the first time, we can prove that the membrane is stiffer and the process is slower."
The World Health Organization (WHO) views the issue of antibacterial resistance as a major threat to public health worldwide, threatening our ability to treat common infectious diseases, leading to illness, disability and death extended. Every year, about 70,000 people worldwide die from drug-resistant bacterial infections, HIV / AIDS, tuberculosis and malaria.
Experts warned that by 2050, the annual death toll would reach 10 million worldwide.
The work was funded by the Canadian Institutes of Health Research (CIHR), the Natural Sciences and Engineering Research Council of Canada (NSERC) and the Canada Foundation for Innovation (CFI).
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Material provided by McMaster University. Note: Content can be changed for style and length.
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