Jessica M A Blair

TL;DR: Recent advances in understanding of the mechanisms by which bacteria are either intrinsically resistant or acquire resistance to antibiotics are reviewed, including the prevention of access to drug targets, changes in the structure and protection of antibiotic targets and the direct modification or inactivation of antibiotics.

TL;DR: The role of efflux in resistance of clinical isolates of Gram-negative bacteria, the regulatory mechanisms that control efflux pump expression, the recent advances in understanding ofefflux pump structure are discussed, and how inhibition of Efflux is a promising future strategy for tackling multidrug resistance in Gram- negative pathogens are discussed.

TL;DR: The recent structure of an assembled tripartite system, AcrAB-TolC, revealed that AcrB is docked onto TolC, which remains in an open state once part of the assembled complex and three AcrA molecules complete the structure, in contrast to data for the MexAB-OprM system of P. aeruginosa.

TL;DR: Rec recreation of the mutation in standard Escherichia coli and Salmonella strains showed that G288D AcrB altered substrate specificity, conferring decreased susceptibility to the fluoroquinolone antibiotic ciprofloxacin by increased efflux, and increased susceptibility to other drugs by decreased efflux.

TL;DR: It is demonstrated that AcrA, AcrB, and TolC are each required for efficient adhesion to and invasion of epithelial cells and macrophages by Salmonella in vitro.