ReviewClinical reviews in allergy & immunology2008
Chronic inflammation in the cystic fibrosis lung: alterations in inter- and intracellular signaling.
Review in Clinical reviews in allergy & immunology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 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
69 citing papers in PubMed, 141 citations in OpenAlex.
- The Involvement of MicroRNAs in Innate Immunity and Cystic Fibrosis Lung Disease: A Narrative Review.Current issues in molecular biology · 2026Review
- Genome-wide association study of susceptibility toThe European respiratory journal · 2024Article
- Review
- Laboratory Tools to Predict CFTR Modulator Therapy Effectiveness and to Monitor Disease Severity in Cystic Fibrosis.Journal of personalized medicine · 2024Review
- Pathogenesis ofInfection and immunity · 2023Article
- Inflammatory Activity of Epithelial Stem Cell Variants from Cystic Fibrosis Lungs Is Not Resolved by CFTR Modulators.American journal of respiratory and critical care medicine · 2023Article
- Neutrophil bactericidal activity and host defenses in cystic fibrosis: a narrative review.Journal of thoracic disease · 2023Review
- Fibroblast Growth Factor 23 Signaling Does Not Increase Inflammation fromMedicina (Kaunas, Lithuania) · 2023Article
- The epithelial-mesenchymal plasticity landscape: principles of design and mechanisms of regulation.Nature reviews. Genetics · 2023Review
- Multiomic Investigations into Lung Health and Disease.Microorganisms · 2023Review
- In vivo impact of tubulin polymerization promoting protein (Tppp) knockout to the airway inflammatory response.Scientific reports · 2023Article
- Impact of elexacaftor-tezacaftor-ivacaftor on bacterial colonization and inflammatory responses in cystic fibrosis.Pediatric pulmonology · 2023Article
- Permeability Assessment of a High-Throughput Mucosal Platform.Pharmaceutics · 2023Article
- A cooperativity between virus and bacteria during respiratory infections.Frontiers in microbiology · 2023Review
- A novel in vitro model to study prolonged Pseudomonas aeruginosa infection in the cystic fibrosis bronchial epithelium.PloS one · 2023Article
- Inflammation and Infection in Cystic Fibrosis: Update for the Clinician.Children (Basel, Switzerland) · 2022Review
- Impact ofInternational journal of molecular sciences · 2022Review
- Chasing a Breath of Fresh Air in Cystic Fibrosis (CF): Therapeutic Potential of Selective HDAC6 Inhibitors to Tackle Multiple Pathways in CF Pathophysiology.Journal of medicinal chemistry · 2022Review
- Network Analysis to Identify Multi-Omic Correlations in the Lower Airways of Children With Cystic Fibrosis.Frontiers in cellular and infection microbiology · 2022Article
- Review
9 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
3 authors at 2 institutions in 1 country.
Funding
Abstract
A vicious cycle of airway obstruction, infection, and inflammation continues to cause most of the morbidity and mortality in cystic fibrosis (CF). Mutations that result in decreased expression or function of the membrane Cl(-) channel, cystic fibrosis transmembrane regulator (CFTR), result in a decrease in the volume (and hence the depth) of liquid on the airway surface, impaired ciliary function, and dehydrated glandular secretions. In turn, these abnormalities contribute to a milieu, which promotes chronic infection with a limited but unique spectrum of microorganisms. Defects in CFTR also perturb regulation of several intracellular signaling pathways including signal transducers and activator of transcription, I-kappaB and nuclear factor-kappa B, and low molecular weight GTPases. Together, these abnormalities result in excessive production of NF-kappaB dependent cytokines such as interleukin (IL)-1, tumor necrosis factor (TNF), IL-6, and IL-8. There are decreased responses to interferon gamma and transforming growth factor beta leading to decreased production of iNOS and NO. Abnormalities of lipid mediators and decreased secretion of counter/regulatory cytokines have also been reported. Together, these effects combine to create a chronic inflammatory process, which damages and obstructs the airways, and eventually claims the life of the patient.
Indexed as
Identifiers
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.