Breakthrough research could rescue antibiotic of last resort

10 April 2017

New study by UCLan senior lecturer features in Nature’s Scientific Reports

Researchers have discovered how some superbugs, including MRSA, meningitis and pneumonia, can become resistant to one of the key antibiotics of last resort, marking a significant leap forward in the global fight against antibiotic resistance.

The study, published today (11 April) in Nature’s Scientific Reports, has shown that a specific protein, known as VanS, binds with Vancomycin – one of the antibiotics of last resort. This discovery offers crucial new insight into the mechanisms involved in activating resistance genes in some of the most difficult-to-treat and deadly infections, including penicillin-resistant pneumonia and MRSA, one of the most serious hospital-acquired infections.

This breakthrough discovery was found by researchers at the University of Central Lancashire (UCLan) and the University of Nottingham.

"We’ve identified that the important antibiotic known as Vancomycin binds directly to a specific protein in the membrane of some key bacteria."

‘Antibiotics of last resort’ are used to tackle serious and multi-drug-resistant infections when other potential treatments have failed. Since some bacterial strains are now also evolving to become resistant to this last line of defence, fundamental research which addresses how this antibiotic resistance is triggered is crucial to address this global issue.

It is estimated that antimicrobial resistance, which renders existing antibiotics useless against some bacterial infections, will lead to the loss of 10 million lives a year by 2050 and cost £69tn per year globally. This is according to the Review on Antimicrobial Resistance published in 2016*, which highlights the severity of the issue.

Dr Mary Phillips-Jones, director of the study and Senior Lecturer in Biochemistry and Microbiology at UCLan, said: “We’ve identified that the important antibiotic known as Vancomycin binds directly to a specific protein in the membrane of some key bacteria. We believe this may then trigger the resistance mechanism, most likely in combination with other additional factors.

“Understanding how these ‘resistance triggering’ mechanisms work in bacteria means that we can find new ways of destroying them, taking us one step closer towards combating these harmful superbugs.”

"Understanding how these ‘resistance triggering’ mechanisms work in bacteria means that we can find new ways of destroying them, taking us one step closer towards combating these harmful superbugs."

Stephen Harding, co-director of the study and Professor of Applied Biochemistry at the University of Nottingham, said: “Many bacteria are very clever in quickly adapting to defend against the medicines used to kill them. Identifying the key interaction point is a major step in helping us to permanently outwit them.”

The work was carried out at UCLan and the University of Nottingham and also utilised facilities made available at the University of Leeds and the Diamond Light Source Ltd, Oxfordshire. The study was supported financially by UCLan’s School of Pharmacy and Biomedical Sciences and the National Centre for Macromolecular Hydrodynamics at the University of Nottingham.