Scientists found a new way to cut antibiotic resistance and help curb superbugs

In a bid to fend off dangerous bacteria.
Derya Ozdemir
Enterobacteria.Scharvik/iStock

Infections caused by antibiotic-resistant bacteria now kill more than a million people worldwide each year, which is higher than the number of people killed each year by HIV/AIDS or malaria.

This growing health crisis may have just received a significant aid thanks to a group of scientists who believe they have discovered a novel strategy to combat antibiotic-resistant bacteria.

The researchers, led by Despoina Mavridou of The University of Texas, found a new way to reduce antibiotic resistance in bacteria that cause human diseases, such as E. coli, K. pneumoniae and P. aeruginosa. These bacteria are responsible for the bulk of antibiotic-resistant infections.

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The researchers were able to make the bacteria susceptible to antibiotics once more by blocking a key protein that drives the development of resistance capabilities inside the bacteria.

Understanding drug-resistant bacteria

Bacteria are growing increasingly resistant to currently available antibiotics, and as we use more antibiotics, the more resistant the bacteria can become. One of the reasons why this happens is, when sensitive bacteria are killed, stronger germs resist the treatment and thrive and reproduce. Frequent and improper antibiotic use also contributes to this complicated process.

Scientists have been trying to develop new drugs to fight these bacteria; however, the discovery of new antibiotics is challenging, which leaves many people, both from high and low-income backgrounds, vulnerable to superbugs, which have a slew of proteins in their arsenals that destroy antibiotics.

For this process to work, these proteins must be folded into the correct forms. Now, researchers have discovered that yet another protein, named DsbA, helps fold the proteins into those shapes.

Changing the curve

According to the study newly published in the journal eLife, the researchers used chemicals that cannot be used directly in human patients to block DsbA. Other efforts have focused on blocking resistance proteins, but this is the first time a group of researchers has been able to prevent resistance proteins from forming in the first place.

"Our findings show that by targeting disulfide bond formation and protein folding, it is possible to reverse antibiotic resistance across several major pathogens and resistance mechanisms," said Christopher Furniss, one of the lead authors of this study at Imperial College London, in a press release. "This means that the development of clinically useful DsbA inhibitors in the future could offer a new way to treat resistant infections using currently available antibiotics."

The next step for the researchers is to find inhibitors that can produce the same results while being safe to employ in humans, hopefully prolonging the lifespan of existing antimicrobials.

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