ArticleCell2018
Drug-Driven Phenotypic Convergence Supports Rational Treatment Strategies of Chronic Infections.
Article in Cell, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 105 papers.
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Who cites it
105 citing papers in PubMed.
- Efflux modulation as an antimicrobial strategy: mechanisms and translational perspectives.npj drug discovery · 2026Review
- Collateral sensitivity-harnessing microbial vulnerabilities as a solution to antimicrobial resistance.Molecular biology reports · 2026Review
- Phenotypic convergence and collateral susceptibility development in Pseudomonas aeruginosa under antibiotic exposure in ICU patients.npj antimicrobials and resistance · 2026Article
- Evolutionary drivers of divergent collateral sensitivity responses during antibiotic therapy.Nature ecology & evolution · 2026Review
- EGFR inhibitor-resistant lung cancers exhibit collateral sensitivity to a covalent, cysteine-independent KEAP1 oligomerizing molecular bridge.Nature communications · 2026Article
- Linezolid and levofloxacin: an uncommon pairing that suppresses evolution of resistance inFEMS microbes · 2026Article
- Within-host adaptation mutations associated with persistent colonization ofFrontiers in cellular and infection microbiology · 2026Article
- Evolutionary trajectories determine feasibility of collateral sensitivity-based antibiotic treatment strategies in critical bacterial pathogens.Communications biology · 2025Article
- Computational framework for streamlining the success of sequential antibiotic therapy.npj antimicrobials and resistance · 2025Article
- Invariant set theory for predicting potential failure of antibiotic cycling.Infectious Disease Modelling · 2025Article
- Vancomycin Sensitization inACS infectious diseases · 2025Article
- Cross-talk between Pseudomonas aeruginosa and urinary tract infections.World journal of urology · 2025Review
- Ciprofloxacin resistance rapidly declines in nfxB defective clinical strains of Pseudomonas aeruginosa.Nature communications · 2025Article
- Ceftazidime-avibactam use selects multidrug-resistance and prevents designing collateral sensitivity-based therapies against Pseudomonas aeruginosa.Nature communications · 2025Article
- Leveraging collateral sensitivity to counteract the evolution of bacteriophage resistance in bacteria.mLife · 2025Article
- Targeting efflux pumps prevents the multi-step evolution of high-level resistance to fluoroquinolone inMicrobiology spectrum · 2025Article
- Quantitative analysis of relationship between mutation rate and speed of adaptation under antibiotic exposure in Escherichia coli.PLoS genetics · 2025Article
- Dynamic collateral sensitivity profiles highlight opportunities and challenges for optimizing antibiotic treatments.PLoS biology · 2025Article
- Systematic mapping of antibiotic cross-resistance and collateral sensitivity with chemical genetics.Nature microbiology · 2025Article
- Article
45 more citing papers are in PubMed but not listed here.
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chronic Pseudomonas aeruginosa infections evade antibiotic therapy and are associated with mortality in cystic fibrosis (CF) patients. We find that in vitro resistance evolution of P. aeruginosa toward clinically relevant antibiotics leads to phenotypic convergence toward distinct states. These states are associated with collateral sensitivity toward several antibiotic classes and encoded by mutations in antibiotic resistance genes, including transcriptional regulator nfxB. Longitudinal analysis of isolates from CF patients reveals similar and defined phenotypic states, which are associated with extinction of specific sub-lineages in patients. In-depth investigation of chronic P. aeruginosa populations in a CF patient during antibiotic therapy revealed dramatic genotypic and phenotypic convergence. Notably, fluoroquinolone-resistant subpopulations harboring nfxB mutations were eradicated by antibiotic therapy as predicted by our in vitro data. This study supports the hypothesis that antibiotic treatment of chronic infections can be optimized by targeting phenotypic states associated with specific mutations to improve treatment success in chronic infections.
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