0000000000324789

AUTHOR

Arnaud Bolard

showing 2 related works from this author

The Efflux Pump MexXY/OprM Contributes to the Tolerance and Acquired Resistance of Pseudomonas aeruginosa to Colistin

2020

The intrinsic resistance of Pseudomonas aeruginosa to polymyxins in part relies on the addition of 4-amino-4-deoxy-l-arabinose (Ara4N) molecules to the lipid A of lipopolysaccharide (LPS), through induction of operon arnBCADTEF-ugd (arn) expression. As demonstrated previously, at least three two-component regulatory systems (PmrAB, ParRS, and CprRS) are able to upregulate this operon when bacteria are exposed to colistin. In the present study, gene deletion experiments with the bioluminescent strain PAO1::lux showed that ParRS is a key element in the tolerance of P. aeruginosa to this last-resort antibiotic (i.e., resistance to early drug killing). Other loci of the ParR regulon, such as th…

medicine.drug_classOperonPolymyxinMutantMicrobial Sensitivity Testsmedicine.disease_causeMicrobiologyLipid A03 medical and health sciencesBacterial ProteinsMechanisms of ResistanceDrug Resistance BacterialmedicinePharmacology (medical)ComputingMilieux_MISCELLANEOUS030304 developmental biologyPharmacology0303 health sciencesColistin030306 microbiologyPseudomonas aeruginosaChemistryMembrane Transport ProteinsGene Expression Regulation BacterialAnti-Bacterial AgentsInfectious DiseasesRegulonPseudomonas aeruginosa[SDE]Environmental SciencesColistinlipids (amino acids peptides and proteins)EffluxGene DeletionBacterial Outer Membrane Proteinsmedicine.drugAntimicrobial Agents and Chemotherapy
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Production of Norspermidine Contributes to Aminoglycoside Resistance in pmrAB Mutants of Pseudomonas aeruginosa

2019

Emergence of resistance to polymyxins in Pseudomonas aeruginosa is mainly due to mutations in two-components systems, that promote addition of 4-amino-4-deoxy-L-arabinose to the lipopolysaccharide (LPS) through upregulation of operon arnBCADTEF-ugd (arn) expression. Here, we demonstrate that mutations occurring in different domains of histidine kinase PmrB or in response regulator PmrA result in coresistance to aminoglycosides and colistin. All seventeen clinical strains tested exhibiting such a cross-resistance phenotype were found to be pmrAB mutants. As shown by gene deletion experiments, the decreased susceptibility of the mutants to aminoglycosides was independent from operon arn but r…

Spectrometry Mass Electrospray IonizationOperonSpermidineMutantMicrobial Sensitivity TestsMicrobiology03 medical and health scienceschemistry.chemical_compoundBacterial ProteinsMechanisms of Resistance[SDV.BBM.GTP]Life Sciences [q-bio]/Biochemistry Molecular Biology/Genomics [q-bio.GN]PolyaminesPharmacology (medical)GeneComputingMilieux_MISCELLANEOUS030304 developmental biologyPharmacology0303 health sciences030306 microbiologyColistinNorspermidineHistidine kinaseGene Expression Regulation Bacterial[SDV.MP.BAC]Life Sciences [q-bio]/Microbiology and Parasitology/BacteriologyAnti-Bacterial AgentsResponse regulatorInfectious DiseasesAminoglycosideschemistryPseudomonas aeruginosaEffluxBacterial outer membraneTranscription Factors
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