ReviewClinical reviews in allergy & immunology2008
Anti-inflammatory therapies for cystic fibrosis-related lung disease.
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 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
15 citing papers in PubMed, 42 citations in OpenAlex.
- Synergistic Antimicrobial Effects of Ibuprofen Combined with Standard-of-Care Antibiotics against Cystic Fibrosis Pathogens.Biomedicines · 2023Article
- Article
- Dysfunctional Inflammation in Cystic Fibrosis Airways: From Mechanisms to Novel Therapeutic Approaches.International journal of molecular sciences · 2021Review
- Antimicrobial Activity of Ibuprofen against Cystic Fibrosis-Associated Gram-Negative Pathogens.Antimicrobial agents and chemotherapy · 2018Article
- Human Cellular Models for the Investigation of Lung Inflammation and Mucus Production in Cystic Fibrosis.Analytical cellular pathology (Amsterdam) · 2018Review
- Ibuprofen regulation of microtubule dynamics in cystic fibrosis epithelial cells.American journal of physiology. Lung cellular and molecular physiology · 2016Article
- Antimicrobial Properties of Mesenchymal Stem Cells: Therapeutic Potential for Cystic Fibrosis Infection, and Treatment.Stem cells international · 2016Article
- Current Concepts and Controversies in Innate Immunity of Cystic Fibrosis Lung Disease.Journal of innate immunity · 2016Review
- Anchored PDE4 regulates chloride conductance in wild-type and ΔF508-CFTR human airway epithelia.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2014Article
- Article
- The immunomodulatory effect of inhaled granulocyte-macrophage colony-stimulating factor in cystic fibrosis. A new treatment paradigm.Journal of inflammation research · 2012Article
- Bergamot (Citrus bergamia Risso) fruit extracts and identified components alter expression of interleukin 8 gene in cystic fibrosis bronchial epithelial cell lines.BMC biochemistry · 2011Article
- Phospholipase C-β3 is a key modulator of IL-8 expression in cystic fibrosis bronchial epithelial cells.Journal of immunology (Baltimore, Md. : 1950) · 2011Article
- Pharmacological correction of a defect in PPAR-gamma signaling ameliorates disease severity in Cftr-deficient mice.Nature medicine · 2010Article
- Regulation of ENaC-Mediated Sodium Reabsorption by Peroxisome Proliferator-Activated Receptors.PPAR research · 2010Article
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
Cystic fibrosis (CF) is an autosomal recessive disease affecting many organ systems. In the lung, the underlying ion transport defect in CF establishes a perpetuating cycle of impaired airway clearance, chronic endobronchial infection, and exuberant inflammation. The interrelated nature of these components of CF lung disease makes it likely that the most effective therapeutic strategies will include treatments of each of these. This chapter reviews the preclinical and clinical data focused on ways to better understand and particularly to limit inflammation in the CF airway. Anti-inflammatories are an attractive therapeutic target in CF with a proven ability to decrease the rate of decline in lung function. However, the inherent complexity of the inflammatory response combined with the obvious dependency on this response to contain infection and the side effect profiles of common anti-inflammatories have made identifying the most suitable agents challenging. Research continues to discover impairments in signaling events in CF that may contribute to the excessive inflammation seen clinically. Concurrent with these findings, promising new therapies are being evaluated to determine which agents will be most effective and well tolerated. Available data from studies commenced over the last two decades, which have generated both encouraging and disappointing results, are reviewed below.
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.