The discovery of a new mechanism of resistance to common antibiotics could pave the way for improved treatments for harmful bacterial infections, a study suggests.

Targeting this defence mechanism could aid efforts to combat antimicrobial resistance (AMR), one of the world’s most urgent health challenges, researchers say.

Findings from the study reveal how a repair system inside some bacteria plays a pivotal role in helping them survive commonly-used antibiotics.

Many of these drugs work by targeting the production of proteins essential for bacterial growth and survival.

Now, researchers from the University of Edinburgh have identified new drug targets within a special repair system possessed by certain bacteria, known as Rtc, which enables them to counteract the effects of these antibiotics.

Rtc acts to repair a bacteria’s damaged RNA, the molecule essential for translating genetic information held in DNA into functional proteins inside cells, allowing it to maintain protein production and growth even in the presence of antibiotics, the team says.

A key finding of the work was that bacterial responses to antibiotics can be unpredictable, as the expression of the Rtc repair system varies from cell to cell.

This could explain why some infections are so difficult to treat, as some bacteria can survive antibiotic treatment better than others, the team says.

Researchers made the discovery using a combination of computer models and lab experiments involving E. coli, which is known to develop resistance to antibiotics.

Their findings suggest that tailoring treatments to target key components of the Rtc repair system could improve the effectiveness of existing antibiotics, making them more capable of eradicating infections.

The study not only highlights the complexity of bacterial survival strategies but also opens new avenues for the development of therapies that are more effective at tackling AMR, the team says.

The findings are published in the journal Nature Communications. The research, which also involved scientists from Queen Mary University of London and Imperial College London, was supported by the Biotechnology and Biological Sciences Research Council, Leverhulme Trust and Wellcome.

Dr Andrea Weisse, of the University of Edinburgh’s Schools of Biological Sciences and Informatics, who led the study, said: “Bacteria are clever little things. They have been learning how to dodge our antibiotics, and they are getting better at it all the time. If we don’t find new drugs – or new tricks to outsmart them – we are in trouble. What we are trying to do here is really understand how their defence systems work. Once we see the mechanism clearly, we can figure out smarter ways to beat them and treat infections more effectively.”