Scientists at the University of East Anglia are getting closer to solving the problem of antibiotic resistance. New research published today in the journal Nature reveals the mechanism by which drug-resistant bacterial cells maintain a defensive barrier.
The findings pave the way for a new wave of drugs that kill superbugs by bringing down their defensive walls rather than attacking the bacteria itself. It means that in future, bacteria may not develop drug-resistance at all.
Unravelling this mechanism could also help scientists understand more about human cell dysfunctions linked to disorders such as diabetes, Parkinson’s and other neurodegenerative diseases.
The team, supported by the Wellcome Trust, used Diamond Light Source, one of the world’s most advanced scientific machines, to investigate a class of bacteria called ‘Gram-negative bacteria’.
Diamond produces intense light 10 billion times brighter than the sun, allowing scientists to explore almost any material in atomic detail.
Gram-negative bacteria is particularly resistant to antibiotics because of its cells’ impermeable lipid-based outer membrane.
This outer membrane acts as a defensive barrier against attacks from the human immune system and antibiotic drugs. It allows the pathogenic bacteria to survive, but removing this barrier causes the bacteria to become more vulnerable and die.
The research team previously found an ‘Achilles heel’ in this defensive barrier. But exactly how this defensive cell wall is built and maintained – the ‘assembly machinery’ – was unknown until now.
Scientists studied the gram-negative bacteria E.coli, in which the beta-barrel assembly machinery contains five subunits – known as BamA, BamB, BamC, BamD and BamE. They wanted to know exactly how these subunits work together to insert the outer membrane proteins into the outer membrane or cell wall.