ArticleThe ISME journal2026
Microenvironmental effects of a non-antibiotic therapy for a chronic Polymicrobial infection Alter microbial physiology, competition, and virulence.
Article in The ISME journal, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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.
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.
Who cites it
2 citing papers in PubMed.
- Differential Metabolite Production Underlies Disruption of the Cystic Fibrosis Airway Microbiota by Pathogens.bioRxiv : the preprint server for biology · 2026Article
- Small is big: growing impact of small molecule mass spectrometry in infectious disease drug development.mSphere · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
19 authors.
Funding
Abstract
People with cystic fibrosis (pwCF) have reduced mucociliary clearance in their airways, leading to the build-up of thick, sticky mucus susceptible to opportunistic infection. A new treatment, comprised of three small molecule drugs called Elexacaftor/Tezacaftor/Ivacaftor (ETI), has improved mucociliary clearance and lung function in pwCF, but how this therapy alters lung infections is poorly understood. This study experimentally modeled the biochemical changes in airway mucus caused by ETI to determine its effect on the CF lung microbiome structure and function. We prepared Artificial Sputum Medium (ASM) with reduced primary carbon sources (amino acids, deoxyribonucleic acid DNA, and mucin) to mimic the effects of ETI on mucus biochemistry due to improved mucociliary clearance and reduced pulmonary inflammation. The control and modified ASM were inoculated with pure CF pathogens or mixed-species communities and then grown in oxic and anoxic conditions, followed by multi-omics data analysis. Although oxygen strongly altered the community structure, the nutrient depletions in ASM had little effect. Instead, the reduced carbon sources altered the physiology of the collective community and its individual pathogens. This included modified growth kinetics in addition to altered nitrogen and nucleotide metabolism. Under reduced amino acid concentrations, a known effect of ETI on the sputum metabolome, the production of both Pseudomonas aeruginosa's quinolones and rhamnolipids was significantly reduced. This indirect effect of ETI translates to reduced killing of competing pathogens and reduced toxicity to epithelial cells isolated from the airways of explanted human lung tissues. These findings indicate that ETI may provide further benefit to pwCF by reducing the competition and virulence of its principal pathogen and highlight how microenvironmental effects can have powerful impacts on polymicrobial infections.
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Registered trials
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