ArticleScientific reports2025
People with cystic fibrosis with high sputum neutrophil elastase on elexacaftor-tezacaftor-ivacaftor exhibit worse pulmonary function and pro-inflammatory airway milieu.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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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.
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Who cites it
3 citing papers in PubMed.
- The cystic fibrosis airway cytokine interleukin-1β enhances cystic fibrosis transmembrane conductance regulator modulator efficacy.ERJ open research · 2026Article
- The primary cilium as a compartmentalized signaling hub in tissue immunity and homeostasis.Frontiers in cell and developmental biology · 2026Review
- The Role of Alpha-1 Antitrypsin in the Pathophysiology and Treatment of Inflammatory Lung Diseases.Journal of inflammation research · 2026Review
Corrections and comments
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Authors and funding
10 authors.
Funding
Abstract
Cystic fibrosis (CF) is a genetic condition affecting over 100,000 individuals worldwide. Lung disease is the main cause of mortality in CF, with chronic neutrophilic inflammation as a hallmark. Elexacaftor/tezacaftor/ivacaftor (ETI) is a combination of highly effective CF transmembrane conductance regulator (CFTR) modulators, conferring significant pulmonary gains to treated patients. However, the extent to which ETI controls inflammation is uncertain. To investigate this, we quantified effector proteins, cytokines, and metabolites in sputum fluid supernatant from ETI-treated (n = 32) and treatment-naïve (n = 9) people with CF (pwCF). ETI-treated pwCF showed detectible ivacaftor and tezacaftor in sputum, and overall lower sputum neutrophil elastase (NE) activity than ETI-naïve pwCF, although they displayed a clear bimodal distribution [NE
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Registered trials
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