Evidence map›Paper›PMID 38442240›Full record

ArticleThe Journal of infectious diseases2024

Impact of CFTR Modulation on Pseudomonas aeruginosa Infection in People With Cystic Fibrosis.

Emma L Ledger, Daniel J Smith, Jing Jie Teh, Michelle E Wood, Page E Whibley, Mark Morrison, Joanna B Goldberg, David W Reid, Timothy J Wells

Open access · hybridAbstract read
In one paragraph

Article in The Journal of infectious diseases, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
13.4field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

31 citing papers in PubMed, 32 citations in OpenAlex.

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  16. Activation of theInfection and immunity · 2025
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  19. NorA and Tet38 efflux pumps enableAntimicrobial agents and chemotherapy · 2025
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  20. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors at 3 institutions in 2 countries.

Emma L LedgerFrazer Institute, Faculty of Medicine, The University of Queensland, Brisbane, Australia.ORCID 0000-0002-3488-5252
Daniel J SmithNorthside Clinical Unit, The University of Queensland, Brisbane, Australia.
Jing Jie TehFrazer Institute, Faculty of Medicine, The University of Queensland, Brisbane, Australia.ORCID 0000-0002-2914-8901
Michelle E WoodAdult Cystic Fibrosis Centre, The Prince Charles Hospital, Brisbane, Australia.
Page E WhibleyAdult Cystic Fibrosis Centre, The Prince Charles Hospital, Brisbane, Australia.
Mark MorrisonFrazer Institute, Faculty of Medicine, The University of Queensland, Brisbane, Australia.ORCID 0000-0001-9257-9133
Joanna B GoldbergDepartment of Pediatrics, Division of Pulmonary, Asthma, Cystic Fibrosis, and Sleep, Emory University School of Medicine, Atlanta, Georgia, USA.
David W ReidNorthside Clinical Unit, The University of Queensland, Brisbane, Australia.
Timothy J WellsFrazer Institute, Faculty of Medicine, The University of Queensland, Brisbane, Australia.ORCID 0000-0001-7766-5404
The University of Queensland · AUPrince Charles Hospital · AUEmory University · US

Funding

Common Good Prince Charles Hospital Foundation NI2020-61Cystic Fibrosis AustraliaCystic Fibrosis Foundation 00849I221
6 · The paper itself

Abstract

backgroundPseudomonas aeruginosa is a multidrug-resistant pathogen causing recalcitrant pulmonary infections in people with cystic fibrosis (pwCF). Cystic fibrosis transmembrane conductance regulator (CFTR) modulators have been developed that partially correct the defective chloride channel driving disease. Despite the many clinical benefits, studies in adults have demonstrated that while P. aeruginosa sputum load decreases, chronic infection persists. Here, we investigate how P. aeruginosa in pwCF may change in the altered lung environment after CFTR modulation.

methodsP. aeruginosa strains (n = 105) were isolated from the sputum of 11 chronically colonized pwCF at baseline and up to 21 months posttreatment with elexacaftor-tezacaftor-ivacaftor or tezacaftor-ivacaftor. Phenotypic characterization and comparative genomics were performed.

resultsClonal lineages of P. aeruginosa persisted after therapy, with no evidence of displacement by alternative strains. We identified commonly mutated genes among patient isolates that may be positively selected for in the CFTR-modulated lung. However, classic chronic P. aeruginosa phenotypes such as mucoid morphology were sustained, and isolates remained just as resistant to clinically relevant antibiotics.

conclusionsDespite the clinical benefits of CFTR modulators, clonal lineages of P. aeruginosa persist that may prove just as difficult to manage in the future, especially in pwCF with advanced lung disease.

Indexed as

AminophenolsCystic FibrosisCystic Fibrosis Transmembrane Conductance RegulatorDrug CombinationsPseudomonas aeruginosaPseudomonas InfectionsQuinolonesSputumAdultAnti-Bacterial AgentsBenzodioxolesFemaleHumansIndolesMaleMutationAminophenolsAnti-Bacterial AgentsBenzodioxolesCFTR protein, humanCystic Fibrosis Transmembrane Conductance RegulatorDrug Combinationselexacaftor, ivacaftor, tezacaftor drug combinationIndolesPyrazolesPyridinesQuinolinesQuinolonestezacaftor, ivacaftor drug combinationCFTR modulatorscystic fibrosiselexacaftor-tezacaftor-ivacaftorETIPseudomonas aeruginosa

Identifiers

PMID38442240
PMCPMC11420785
OpenAlexW4392444801

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.