CRISPR-Cas9-Based Tool May Help Slow Antimicrobial Resistance Spread
Researchers apply CRISPR-Cas9 editing to bacterial plasmids, exploit bacteria’s immune system
According to the WHO, antimicrobial resistance is a major global threat, with nearly five million deaths annually resulting from antibiotics failing to treat an infection. But a new gene-editing tool that could help reduce the spread of antimicrobial resistance is showing promise.
Bacteria develop resistance when resistant genes are transported between hosts. One way that this occurs is via plasmids—circular strands of DNA, which spread easily between bacteria and swiftly yet autonomously replicate. This can occur in our bodies and environmental settings.
In efforts to address the global crisis, the University of Exeter researchers engineered a plasmid that can specifically target and cut the gene for Gentamicin resistance, harnessing the CRISPR-Cas9 gene editing system.
As published in Microbiology, laboratory experiments found that the plasmid protected its host cell from developing resistance. Furthermore, researchers found that the plasmid effectively targeted antimicrobial-resistant genes in hosts to which it transferred and reversed their resistance.
Lead author David Walker-Sünderhauf, PhD, of the University of Exeter, said, “Antimicrobial resistance threatens to outstrip COVID-19 in terms of the number of global deaths. We urgently need new ways to stop resistance-spreading between hosts. Our technology is showing early promise to eliminate resistance in a wide range of different bacteria. Our next step is to conduct experiments in more complex microbial communities. We hope one day it could be a way to reduce the spread of antimicrobial resistance in environments such as sewage treatment plants, which we know are breeding grounds for resistance.”
- This press release was originally published on the University of Exeter website