ArticleThe Journal of antimicrobial chemotherapy2018
Increased expression of Qnr is sufficient to confer clinical resistance to ciprofloxacin in Escherichia coli.
Article in The Journal of antimicrobial chemotherapy, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 41 citations in OpenAlex.
- Uncommon Pathogens in Common Presentations: Genetic Profiling and Virulence Determinants ofInfectious disease reports · 2025Article
- Antechodynamics and Antechokinetics: Dynamics and Kinetics of Antibiotic Resistance Biomolecules.Biomolecules · 2025Review
- Ribosome phenotypes for rapid classification of antibiotic-susceptible and resistant strains of Escherichia coli.Communications biology · 2025Article
- Combined effects of ciprofloxacin and microplastics on alpine spring water microbiota: evidence from glacier-fed microcosm experiments.Frontiers in microbiology · 2025Article
- The role of prokaryotic argonautes in resistance to type II topoisomerases poison ciprofloxacin.Biochemical Society transactions · 2024Review
- Navigating fluoroquinolone resistance in Gram-negative bacteria: a comprehensive evaluation.JAC-antimicrobial resistance · 2024Review
- QUIRMIA-A Phenotype-Based Algorithm for the Inference of Quinolone Resistance Mechanisms inAntibiotics (Basel, Switzerland) · 2023Article
- Effect of Different Tolerable Levels of ConstitutiveMicrobiology spectrum · 2022Article
- Expression of the qepA1 gene is induced under antibiotic exposure.The Journal of antimicrobial chemotherapy · 2021Article
- Characterization ofIranian journal of veterinary research · 2021Article
- Allogenous Selection of Mutational Collateral Resistance: Old Drugs Select for New Resistance Within Antibiotic Families.Frontiers in microbiology · 2021Review
- Drug-target binding quantitatively predicts optimal antibiotic dose levels in quinolones.PLoS computational biology · 2020Article
- Resistance pattern ofIranian journal of microbiology · 2020Article
- Synergistic Activity of Fluoroquinolones Combining with Artesunate Against Multidrug-ResistantMicrobial drug resistance (Larchmont, N.Y.) · 2020Article
- Transferable Mechanisms of Quinolone Resistance from 1998 Onward.Clinical microbiology reviews · 2019Review
- Resistance and Virulence Mechanisms ofAntimicrobial agents and chemotherapy · 2019Article
- Article
- Multiple Benefits of Plasmid-Mediated Quinolone Resistance Determinants inFrontiers in microbiology · 2019Article
- Alternations in DNA gyrase genes in low-level fluoroquinolone-resistantInfection and drug resistance · 2018Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Ciprofloxacin, a fluoroquinolone, targets two essential bacterial enzymes, DNA gyrase and topoisomerase IV. Plasmid-borne qnr genes, encoding proteins that protect DNA gyrase and topoisomerase IV from inhibition by fluoroquinolones, contribute to resistance development. However, the presence of a plasmid-borne qnr gene alone is insufficient to confer clinical resistance. Objectives: We asked whether the level of expression of qnr was a limiting factor in its ability to confer clinical resistance and whether expression could be increased without reducing fitness or viability. Methods: qnrB and qnrS were recombineered onto the chromosome of Escherichia coli under the control of constitutive promoters of various strengths. Expression was measured by qPCR, MIC and relative fitness as a function of expression level were determined. Results: For both qnr genes there was a positive relationship between the level of qnr mRNA and the MIC of ciprofloxacin. The highest MICs achieved with qnrB or qnrS as the sole resistance determinant were 0.375 and 1 mg/L, respectively, and were reached at expression levels that did not affect growth rate or viability. The qnrS-mediated MIC is above the EUCAST clinical breakpoint for resistance to ciprofloxacin. In the absence of Lon protease activity, overexpression of qnr genes was associated with high fitness cost, possibly explaining observations of toxicity in other genetic backgrounds. Conclusions: The ability to generate a high MIC without incurring a fitness cost shows that, in an appropriate genetic context, qnrS has the potential to generate clinical resistance to ciprofloxacin in one step.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.