ArticleJournal of leukocyte biology2012
Absence of the cystic fibrosis transmembrane regulator (Cftr) from myeloid-derived cells slows resolution of inflammation and infection.
Article in Journal of leukocyte biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 89 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
89 citing papers in PubMed, 139 citations in OpenAlex.
- Cystic fibrosis transmembrane conductance regulator recruitment to phagosomes in neutrophils.Journal of innate immunity · 2013Trial
- Considerations for early life genetic therapies in cystic fibrosis.American journal of physiology. Lung cellular and molecular physiology · 2026Review
- Intrinsic neutrophil dysregulation in programmed cell death promotes neutrophilic inflammation in cystic fibrosis.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2026Article
- The Involvement of MicroRNAs in Innate Immunity and Cystic Fibrosis Lung Disease: A Narrative Review.Current issues in molecular biology · 2026Review
- CFTR negatively reprograms Th2 cell responses, and CFTR potentiation restrains allergic airway inflammation.JCI insight · 2025Article
- Innate Immunity in Cystic Fibrosis: Varied Effects of CFTR Modulator Therapy on Cell-to-Cell Communication.International journal of molecular sciences · 2025Review
- How Effectively Can Oxidative Stress and Inflammation Be Reversed When CFTR Function Is Pharmacologically Improved?Antioxidants (Basel, Switzerland) · 2025Review
- Polymerized cyclodextrin microparticles for sustained antibiotic delivery in lung infections.Journal of biomedical materials research. Part A · 2024Article
- Analysis of CFTR mRNA and Protein in Peripheral Blood Mononuclear Cells via Quantitative Real-Time PCR and Western Blot.International journal of molecular sciences · 2024Article
- Abnormal functional lymphoid tolerance and enhanced myeloid exocytosis are characteristics of resting and stimulated PBMCs in cystic fibrosis patients.Frontiers in immunology · 2024Article
- A minimally invasive bronchoscopic approach for direct delivery to murine airways and application to models of pulmonary infection.Laboratory animals · 2023Article
- Sputum from People with Cystic Fibrosis Reduces the Killing of Methicillin-ResistantPathogens (Basel, Switzerland) · 2023Article
- CFTR dysfunction in smooth muscle drives TGFβ dependent airway hyperreactivity.Respiratory research · 2023Article
- Identification of Virulence Factors Involved in a Murine Model of Severe Achromobacter xylosoxidans Infection.Infection and immunity · 2023Article
- Dysfunctions of Neutrophils in the Peripheral Blood of Children with Cystic Fibrosis.Biomedicines · 2023Article
- CAGE sequencing reveals CFTR-dependent dysregulation of type I IFN signaling in activated cystic fibrosis macrophages.Science advances · 2023Article
- Cystic fibrosis macrophage function and clinical outcomes after elexacaftor/tezacaftor/ivacaftor.The European respiratory journal · 2023Article
- Revisiting Host-Pathogen Interactions in Cystic Fibrosis Lungs in the Era of CFTR Modulators.International journal of molecular sciences · 2023Review
- Article
- Cystic Fibrosis Bone Disease: The Interplay between CFTR Dysfunction and Chronic Inflammation.Biomolecules · 2023Review
29 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
4 authors at 1 institution in 1 country.
Funding
Abstract
The absence or reduction of CFTR function causes CF and results in a pulmonary milieu characterized by bacterial colonization and unresolved inflammation. The ineffectiveness at controlling infection by species such as Pseudomonas aeruginosa suggests defects in innate immunity. Macrophages, neutrophils, and DCs have all been shown to express CFTR mRNA but at low levels, raising the question of whether CFTR has a functional role in these cells. Bone marrow transplants between CF and non-CF mice suggest that these cells are inherently different; we confirm this observation using conditional inactivation of Cftr in myeloid-derived cells. Mice lacking Cftr in myeloid cells overtly appear indistinguishable from non-CF mice until challenged with bacteria instilled into the lungs and airways, at which point, they display survival and inflammatory profiles intermediate in severity as compared with CF mice. These studies demonstrate that Cftr is involved directly in myeloid cell function and imply that these cells contribute to the pathophysiological phenotype of the CF lung.
Indexed as
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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.