ArticleeLife2020
Different CFTR modulator combinations downregulate inflammation differently in cystic fibrosis.
Article in eLife, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05752019 (TAAI Erasmus Research Initiative to Fight CF), which is not on this map. Cited by 64 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.
TAAI Erasmus Research Initiative to Fight CF: Monitoring Inflammation in CF Lung Disease Into a New Era
Who cites it
64 citing papers in PubMed, 102 citations in OpenAlex.
- Ivacaftor Reduces Inflammatory Mediators in Upper Airway Lining Fluid From Cystic Fibrosis Patients With a G551D Mutation: Serial Non-Invasive Home-Based Collection of Upper Airway Lining Fluid.Frontiers in immunology · 2021Trial
- Alveolar macrophage subtypes express cholesterol and inflammation genes in cystic fibrosis.Life science alliance · 2026Article
- Functional Rescue of CFTR-Dependent Transport in a Pancreatic Ductal Epithelial Cell Model: The Impact of Pharmacological Modulation and Inflammation.International journal of molecular sciences · 2026Article
- Article
- Genetic and chemical correction of cystic fibrosis reduces airway susceptibility to SARS-CoV-2.American journal of physiology. Lung cellular and molecular physiology · 2026Article
- Repurposing ivacaftor to attenuate LPS-induced acute lung injury: evidence from a non-cystic fibrosis model.Frontiers in pharmacology · 2026Article
- Article
- Comparison of the Effect of CFTR ModulatorsJournal of clinical medicine · 2025Article
- CFTR Modulators Counteract F508del CFTR Functional Defects in a Pancreatic Epithelial Model of Cystic Fibrosis.Life (Basel, Switzerland) · 2025Article
- Pseudomonas infections persisting after CFTR modulators are widespread throughout the lungs and drive lung inflammation.Cell host & microbe · 2025Article
- Deleterious effect ofERJ open research · 2025Article
- The Role of Triple CFTR Modulator Therapy in Reducing Systemic Inflammation in Cystic Fibrosis.Lung · 2025Article
- Innate Immunity in Cystic Fibrosis: Varied Effects of CFTR Modulator Therapy on Cell-to-Cell Communication.International journal of molecular sciences · 2025Review
- Neutrophil extracellular traps and interleukin-1β in cystic fibrosis lung disease.Frontiers in immunology · 2025Review
- Neutrophil elastase activates macrophage calpain as a mechanism for phagocytic failure.American journal of physiology. Lung cellular and molecular physiology · 2025Article
- The effect of triple CFTR modulator therapy and azithromycin on ion channels and inflammation in cystic fibrosis.ERJ open research · 2024Article
- Article
- The ageing of people living with cystic fibrosis: what to expect now?European respiratory review : an official journal of the European Respiratory Society · 2024Review
- Allergic Bronchopulmonary Aspergillosis (ABPA) in the Era of Cystic Fibrosis Transmembrane Conductance Regulator (CFTR) Modulators.Journal of fungi (Basel, Switzerland) · 2024Review
- CFTR is required for zinc-mediated antibacterial defense in human macrophages.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
4 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors at 3 institutions in 2 countries.
Funding
Abstract
Previously, we showed that serum and monocytes from patients with CF exhibit an enhanced NLRP3-inflammasome signature with increased IL-18, IL-1β, caspase-1 activity and ASC speck release (Scambler et al. eLife 2019). Here we show that CFTR modulators down regulate this exaggerated proinflammatory response following LPS/ATP stimulation. In vitro application of ivacaftor/lumacaftor or ivacaftor/tezacaftor to CF monocytes showed a significant reduction in IL-18, whereas IL-1β was only reduced with ivacaftor/tezacaftor. Thirteen adults starting ivacaftor/lumacaftor and eight starting ivacaftor/tezacaftor were assessed over three months. Serum IL-18 and TNF decreased significantly with treatments, but IL-1β only declined following ivacaftor/tezacaftor. In (LPS/ATP-stimulated) PBMCs, IL-18/TNF/caspase-1 were all significantly decreased and IL-10 was increased with both combinations. Ivacaftor/tezacaftor alone showed a significant reduction in IL-1β and pro-IL-1β mRNA. This study demonstrates that these CFTR modulator combinations have potent anti-inflammatory properties, in addition to their ability to stimulate CFTR function, which could contribute to improved clinical outcomes.
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What OpenQuestion holds
Registered trials
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.