ReviewRespiratory research2003
State of the art: why do the lungs of patients with cystic fibrosis become infected and why can't they clear the infection?
Review in Respiratory research, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT02315547 (Guangzhou Institute of Respiratory Disease), which is not on this map. Cited by 114 papers, 2 of them syntheses that pooled it.
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.
Guangzhou Institute of Respiratory Disease
Who cites it
114 citing papers in PubMed, 2 syntheses or guidelines pooled it, 251 citations in OpenAlex.
- The Human Respiratory Microbiome: Current Understandings and Future Directions.American journal of respiratory cell and molecular biology · 2023Pooled it
- Percutaneous lines for delivering intravenous antibiotics in people with cystic fibrosis.The Cochrane database of systematic reviews · 2010Pooled it
- Mucociliary and long-term particle clearance in airways of patients with immotile cilia.Respiratory research · 2006Trial
- Elastic Fibers in the Pathogenesis of Cystic Fibrosis: Mechanisms, Consequences, and Therapeutic Implications.Life (Basel, Switzerland) · 2026Review
- Opsonization Improves Dual Proteomic Analysis ofJournal of proteome research · 2026Article
- Human infections caused by pathogenic Burkholderia: current clinical challenges and future perspectives.Infection · 2026Review
- Lung organoids as a human system for Mycobacteria infection modeling and drug testing.The FEBS journal · 2026Review
- Essential role of cytochromeFrontiers in cellular and infection microbiology · 2026Article
- Dual-action thioarylamide-based small molecules to target drug-resistant bacteria and chronic inflammation.iScience · 2025Article
- An effective response to respiratory inhibition by aJournal of bacteriology · 2025Article
- Hijacking anaerobic metabolism to restore antibiotic efficacy inApplied and environmental microbiology · 2025Article
- Microbial Contamination of Nebulizers in Patients With Cystic Fibrosis.Turkish archives of pediatrics · 2025Article
- Effects of Several Bile Acids on the Production of Virulence Factors byLife (Basel, Switzerland) · 2024Article
- Article
- Nanoparticles as Drug Delivery Vehicles for People with Cystic Fibrosis.Biomimetics (Basel, Switzerland) · 2024Review
- Comparative microbiome analysis in cystic fibrosis and non-cystic fibrosis bronchiectasis.Respiratory research · 2024Article
- Orphan response regulator NnaR is critical for nitrate and nitrite assimilation inFrontiers in cellular and infection microbiology · 2024Article
- Article
- Review
- Dysfunctions of Neutrophils in the Peripheral Blood of Children with Cystic Fibrosis.Biomedicines · 2023Article
54 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
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cystic Fibrosis (CF) lung disease, which is characterized by airway obstruction, chronic bacterial infection, and an excessive inflammatory response, is responsible for most of the morbidity and mortality. Early in life, CF patients become infected with a limited spectrum of bacteria, especially P. aeruginosa. New data now indicate that decreased depth of periciliary fluid and abnormal hydration of mucus, which impede mucociliary clearance, contribute to initial infection. Diminished production of the antibacterial molecule nitric oxide, increased bacterial binding sites (e.g., asialo GM-1) on CF airway epithelial cells, and adaptations made by the bacteria to the airway microenvironment, including the production of virulence factors and the ability to organize into a biofilm, contribute to susceptibility to initial bacterial infection. Once the patient is infected, an overzealous inflammatory response in the CF lung likely contributes to the host's inability to eradicate infection. In response to increased IL-8 and leukotriene B4 production, neutrophils infiltrate the lung where they release mediators, such as elastase, that further inhibit host defenses, cripple opsonophagocytosis, impair mucociliary clearance, and damage airway wall architecture. The combination of these events favors the persistence of bacteria in the airway. Until a cure is discovered, further investigations into therapies that relieve obstruction, control infection, and attenuate inflammation offer the best hope of limiting damage to host tissues and prolonging survival.
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.