Atomic force microscopy (AFM) has become a powerful tool to provide nanoscale insights into the spatial organization, biomechanics, and intermolecular interactions of the cell envelopes of living bact...

Murepavadin is a Pseudomonas-specific antibiotic that targets LPS transport protein LptD. However, whilst the mode of action of murepavadin is well defined, the mechanism by which the drug gains acces...

Exposée à la polymyxine B, la bactérie tente de se protéger en fabriquant une armure… qui la conduit à sa perte.

The top image shows an untreated E.coli bacterium; the bottom shows a bacterium after 90 minutes of being exposed to the antibiotic polymyxin B Carolina Borrelli, Edward Douglas et al./Nature Microbiology The way antibiotics called polymyxins pierce the armour of bacteria has been revealed in stunning detail by high-resolution microscopy, which could help us develop new treatments for drug-resistant infections. Polymyxins are commonly used as a last-resort treatment against some so-called gram-negative bacteria, which can cause infections such as pneumonia, meningitis and typhoid fever. “The top three World Health Organization priority pathogens are all gram-negative bacteria, and this is largely a reflection of their complex cell envelope,” says…

Nobody expected the bacteria to commit suicide. But that is essentially what happens when polymyxin antibiotics attack, according to stunning new microscopy images that reveal how these last-resort drugs actually work after 80 years of clinical mystery. Researchers at University College London and Imperial College London have captured the first real-time images of polymyxin B piercing bacterial defenses, and the mechanism turns out to be far stranger than anyone predicted.

A team led by UCL (University College London) and Imperial College London researchers has shown for the first time how life-saving antibiotics called polymyxins pierce the armor of harmful bacteria.

The antibiotic polymyxin B requires bacterial metabolic activity to cause sufficient damage to the outer membrane to access the inner membrane, which it permeabilizes via an energy-independent mechanism to kill the cell.