ReviewMediators of inflammation1999
Inflammation and CFTR: might neutrophils be the key in cystic fibrosis?
Review in Mediators of inflammation, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT04970225 (Functional and Phenotypic Characteristics of Blood Neutrophils in Cystic Fibrosis), which is not on this map. Cited by 15 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.
Functional and Phenotypic Characteristics of Blood Neutrophils in Cystic Fibrosis
Who cites it
15 citing papers in PubMed, 39 citations in OpenAlex.
- Cystic fibrosis transmembrane conductance regulator recruitment to phagosomes in neutrophils.Journal of innate immunity · 2013Trial
- Serum anti-PAD4 autoantibodies are present in cystic fibrosis children and increase with age and lung disease severity.Autoimmunity · 2022Article
- Mucosal Immunity in Cystic Fibrosis.Journal of immunology (Baltimore, Md. : 1950) · 2021Review
- Hyperinflammation and airway surface liquid dehydration in cystic fibrosis: purinergic system as therapeutic target.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2021Review
- Article
- Modulating Innate and Adaptive Immunity by (R)-Roscovitine: Potential Therapeutic Opportunity in Cystic Fibrosis.Journal of innate immunity · 2016Review
- Mechanism of fibroblast inflammatory responses to Pseudomonas aeruginosa elastase.Microbiology (Reading, England) · 2014Article
- Article
- Depletion of the ubiquitin-binding adaptor molecule SQSTM1/p62 from macrophages harboring cftr ΔF508 mutation improves the delivery of Burkholderia cenocepacia to the autophagic machinery.The Journal of biological chemistry · 2013Article
- Neutrophils in the innate immunity conundrum of cystic fibrosis: a CFTR-related matter?Journal of innate immunity · 2013Article
- Contribution by polymorphonucleate granulocytes to elevated gamma-glutamyltransferase in cystic fibrosis sputum.PloS one · 2012Article
- Autophagy stimulation by rapamycin suppresses lung inflammation and infection by Burkholderia cenocepacia in a model of cystic fibrosis.Autophagy · 2011Article
- CFTR inhibition provokes an inflammatory response associated with an imbalance of the annexin A1 pathway.The American journal of pathology · 2010Article
- Inhibition of NFkappaB by the natural product Withaferin A in cellular models of Cystic Fibrosis inflammation.Journal of inflammation (London, England) · 2009Article
- Cystic fibrosis in adults: current and future management strategies.Clinical reviews in allergy & immunology · 2003Review
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 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The aim of this hypothesis is to provide new insights into the still unclear mechanisms governing airway inflammation in cystic fibrosis. Although the genetic basis of cystic fibrosis as well as the molecular structure of cystic fibrosis transmembrane regulator (CFTR), the mutated protein which causes the disease, have been well defined, a clear relationship between the genetic defect and the pulmonary pathophysiology, especially chronic infections and neutrophil-dominated airway inflammation has not been established. Cystic fibrosis is thus a unique pathological situation in that neutrophils can be depicted as both an antiinfectious and a proinflammatory cell. In cystic fibrosis there is an emerging picture of an imbalance between these two roles with both a reduction in the antiinfectious efficacy and an augmentation of the proinflammatory functions. Better knowledge of fundamental defects in neutrophil function in cystic fibrosis as well as a novel cellular function of CFTR, which will be reviewed, will allow identification of potentially new clinical targets and aid selective therapeutic action aimed at counteracting the lethal neutrophil-induced airway inflammation. The rationale for colchicine therapy is a significant example of a drug which might act both at the molecular levels on CFTR expression in epithelial cells and on neutrophils to mediate antiinflammatory effects. Preliminary results are presented in this issue (Med Inflamm 1999; 8: 13-15).
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.