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.

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

Mutations that block assembly of the interlocked RcsF/β barrel protein complex prevent detection of lipopolysaccharide stress and activation of Rcs signal transduction pathway.

A detailed time-series analysis reveals that the interleukin-10 receptor prevents susceptibility to microbiota-driven colonic inflammation that emerges at the time of weaning by directly inhibiting the acquisition of a pro-inflammatory intestinal macrophage phenotype.

The density of the gut microbiota influences the host immune system and adiposity, and can be therapeutically manipulated.

Phenotypic variants that avoid antibiotic accumulation within clonal bacterial populations are a significant contributor to antibiotic treatment failure and can rely on previously unrecognised survival strategies such as fast growth during drug treatment.

In vivo and in vitro approaches uncover a new function for the β-barrel OmpA and reveal how it interacts with the stress sensor lipoprotein RcsF.

The death of bacterial kin cells releases a danger signal that activates a posttranscriptional response in surviving cells, resulting in the rapid elaboration of interbacterial competition factors.

Gut dysbiosis is involved in severe leptospirosis that is related to translocated microbiota-derived lipopolysaccharide.

Bacillus velezensis has broad-spectrum antibacterial activity and can reduce the colonization of Salmonella Typhimurium in the intestinal tract of mice.