Disruption of disulfide bond formation sensitizes resistant Gram-negative bacteria expressing β-lactamases and mobile colistin resistance enzymes to currently available antibiotics.

Resistance genes that spread as a result of the use of an antimicrobial peptide (colistin) in agriculture (MCR) protect bacteria against key components of human and animal immune systems.

Interactions between a mobile resistance gene and chromosomal mutations drive the evolution of high-level antibiotic resistance.

Modulation of cytoplasmic lipopolysaccharide levels sensitises bacteria to polymyxin antibiotics, revealing a novel combination therapeutic approach.

Acquisition of antibiotic resistance plasmids induces collateral sensitivity to clinically relevant antibiotics in Escherichia coli, paving the way for targeted 'anti-plasmid' therapies able to preferentially eliminate plasmid-carrying bacteria.

Outer membrane vesicles serve as decoys to reduce the chance of direct polymyxin B (PMB) binding to cells, which partly explains why many clinical isolates and microbial communities can be protected against PMB treatment.

Dysregulated unsaturated fatty acids and saturated fatty acids contribute to bacterial phenotypic resistance to antibiotics.

Bacterial gut pathogens that invade into host tissues during infection can boost the spread and accumulation of plasmids over time by forming reservoirs containing these plasmids within host tissues.

The peptidoglycan hydrolase activity of Enterococcus faecium secreted antigen A is crucial for cell wall remodeling during bacterial cell separation and generates muropeptides that stimulate host immunity to enhance immune checkpoint inhibitor anti-cancer therapy.