ArticleInfection and immunity2016
Interleukin-17 Pathophysiology and Therapeutic Intervention in Cystic Fibrosis Lung Infection and Inflammation.
Article in Infection and immunity, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 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
37 citing papers in PubMed, 49 citations in OpenAlex.
- Vitamin D inhibits pro-inflammatory cytokines in the airways of cystic fibrosis patients infected by Pseudomonas aeruginosa- pilot study.Italian journal of pediatrics · 2019Trial
- Pseudomonas aeruginosa induces the generation of pathogenic IFNγNature microbiology · 2026Article
- Pediatric cystic fibrosis is associated with type 3 immune response.Molecular biology reports · 2026Article
- Article
- CFTR Modulators Counteract F508del CFTR Functional Defects in a Pancreatic Epithelial Model of Cystic Fibrosis.Life (Basel, Switzerland) · 2025Article
- Studying the efficacy of JBOL volatile components in idiopathic pulmonary fibrosis (IPF) using GC-MS and network pharmacology.Scientific reports · 2025Article
- Proteomics profiling of inflammatory responses to elexacaftor/tezacaftor/ivacaftor in cystic fibrosis.Frontiers in immunology · 2025Article
- Inflammatory response in CF airway epithelial cells: a comparative study of modulators and wild-type CFTR rescue.Frontiers in pharmacology · 2025Article
- The role of T-helper and T regulatory cells in driving neutrophilic and eosinophilic inflammation in bronchiectasis.Frontiers in immunology · 2025Review
- From CFTR to a CF signalling network: a systems biology approach to study Cystic Fibrosis.BMC genomics · 2024Article
- The gut-lung axis: the impact of the gut mycobiome on pulmonary diseases and infections.Oxford open immunology · 2024Review
- Review
- Article
- Integrating airway microbiome and blood proteomics data to identify multi-omic networks associated with response to pulmonary infection.The microbe · 2023Article
- Review
- The Airway Microbiome-IL-17 Axis: a Critical Regulator of Chronic Inflammatory Disease.Clinical reviews in allergy & immunology · 2023Review
- Acinetobacter baumannii reinforces the pathogenesis by promoting IL-17 production in a mouse pneumonia model.Medical microbiology and immunology · 2023Article
- IL-17 Cytokines and Chronic Lung Diseases.Cells · 2022Review
- Ivacaftor Alters Macrophage and Lymphocyte Infiltration in the Lungs Following Lipopolysaccharide Exposure.ACS pharmacology & translational science · 2022Article
- Gearing up for battle: Harnessing adaptive T cell immunity against gram-negative pneumonia.Frontiers in cellular and infection microbiology · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
Cystic fibrosis (CF) is characterized by an excessive neutrophilic inflammatory response within the airway as a result of defective cystic fibrosis transmembrane receptor (CFTR) expression and function. Interleukin-17A induces airway neutrophilia and mucin production associated with Pseudomonas aeruginosa colonization, which is associated with the pathophysiology of cystic fibrosis. The objectives of this study were to use the preclinical murine model of cystic fibrosis lung infection and inflammation to investigate the role of IL-17 in CF lung pathophysiology and explore therapeutic intervention with a focus on IL-17. Cftr-deficient mice (CF mice) and wild-type mice (WT mice) infected with P. aeruginosa had robust IL-17 production early in the infection associated with a persistent elevated inflammatory response. Intratracheal administration of IL-17 provoked a neutrophilic response in the airways of WT and CF animals which was similar to that observed with P. aeruginosa infection. The neutralization of IL-17 prior to infection significantly improved the outcomes in the CF mice, suggesting that IL-17 may be a therapeutic target. We demonstrate in this report that the pathophysiological contribution of IL-17 may be due to the induction of chemokines from the epithelium which is augmented by a deficiency of Cftr and ongoing inflammation. These studies demonstrate the in vivo contribution of IL-17 in cystic fibrosis lung disease and the therapeutic validity of attenuating IL-17 activity in cystic fibrosis.
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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.