Extraordinary pictures show what a common antibiotic does to E. coli
The image of the upper shows an untreated E.coli bacteria; The background shows a bacteria after 90 minutes of exposure to antibiotic polymyxin B
Carolina Borrelli, Edward Douglas and Al./Nature Microbiology
The way in which antibiotics called polymyxins pierce the armor of bacteria have been revealed in amazing details by high -resolution microscopy, which could help us develop new treatments for drug resistant infections.
Polymyxins are commonly used as the latest object treatment against certain so -called Gram -negative bacteria, which can cause infections such as pneumonia, meningitis and typhoid fever. “The three main priority pathogens of the World Health Organization are all Gram -negative bacteria, and this largely reflects their complex cell envelope,” explains Andrew Edwards at the Imperial College of London.
Around their inner cell, these bacteria have an external surface layer containing molecules called lipopolysaccharides, which act as armor. We knew that the polymyxins target this external layer, but how they disturb it exactly and kill bacteria were not understood; Nor was it for the reason why the drugs do not always work.
Now, Edwards and his colleagues have used biochemical experiences and atomic microscopy – in which a needle just a few nanometers wide creates an image of a cell by detecting its shape – to reveal that one of the two types of polymyxin used therapeutically, called Polymyxin B, causes strange eradication to the surface of the grams of the grams of the gram E. coli.
A few minutes after the publication of the protuberances, the bacteria begins to quickly lose its lipopolysaccharides, which the researchers detected in the solution in which it was.
The researchers say that the presence of the antibiotic triggers the bacteria to try to put more and more “bricks” of Lipopolysaccharide in its defensive wall. But as this adds bricks, he also loses some, temporarily leaving the gaps in his defenses which allow the antibiotic to enter and kill him.
“Antibiotics are a bit like a doe foot that helps these bricks get out of the wall,” explains Edwards. “The external membrane does not disintegrate; it does not fall. But there are clearly gaps where the antibiotic can then arrive at the second membrane.”
He and his colleagues also revealed why the antibiotic does not always work: it only affected active and growing bacteria. When bacteria were sleeping, a state they can enter to survive environmental stress such as deprivation of nutrients, polymyxin B was ineffective because it did not produce its armor.
Images of e. Coli exposed to polymyxin B, showing changes to the outer layer of his membrane, from left to right: untreated; bacteria after 15 minutes of exposure to antibiotics; After 30 minutes; after 60 minutes; After 90 minutes
Carolina Borrelli, Edward Douglas et al. / Nature microbiology
However, the researchers found that the supply of sugar to E. coli The cells awakened them from this sleeping state and, in 15 minutes, the production of armor resumed and the cells were killed. The same should be applied to the other antibiotic polymyxin used therapeutically, polymyxin E.
Edwards says that it may be possible to target dormant bacteria by giving people sugars, but there are dangers to wake these pathogens from their sleep. “You don’t necessarily want bacteria to an infection site start to multiply quickly because it has its own drawbacks,” he said. Instead, he adds, it may be possible to combine different drugs to bypass the hibernation state without waking bacteria.
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