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Gossip girl turnaround

Antibiotic resistance has a gossipy trick — a bacterium passes on its resistance secrets to others, and they tell two friends, and they tell two friends and so on. But researchers at University of California-San Diego have found a way to use their gossip chain-mail skills against them.

The research team developed a way of tricking bacteria into fixing themselves.

The solution is a roaming piece of DNA called pPro-MobV. Bacteria happily accept it because it appears as normal, shared DNA. Once inside, it goes to work.

Within the DNA is a CRISPR system that hunts down resistance genes and snips them. As the DNA is swapped, snipping continues.

The results published in Nature journal npj Antimicrobials and Resistance were dramatic, showing a reduction in antibiotic resistant bacteria by up to 100,000 times.

It’s like disarming, rather than killing, an opponent.

Notably, this comes with a delete option to remove the CRISPR, leaving no traces behind, which is imperative if the method is ever used in a non-lab environment.

This could wipe out resistance genes in such environments as hospital pipes and wastewater systems where superbugs can flourish.

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Immune cell sabotage

Antibiotic resistance, a specific type of antimicrobial resistance (AMR), is a growing global health concern. This occurs when bacteria develop resistance to the antibiotics created to kill them.

As antibiotic resistance grows, viruses called bacteriophages that are used to attack bacteria are making their mark as a new method of fighting infections.

The problem is alveolar macrophages, immune cells in the lungs, clean up these viruses before they can do their job.

A group of researchers in Paris, France recently discovered that in mice with complicated lung infections in which the macrophages were active, the phages were gone quickly and the infections remained. But in the mice without the immune cells, the phages were able to completely wipe out the bacteria.

This demonstrates that though microphages help to fight infection, they can also sabotage phage therapy by eliminating helpful viruses.

The paper, published in Nature Communications, says strategies are needed to work around these immune cells in order for phage treatments to succeed against drug-resistant lung infections.

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