ReviewClinical science (London, England : 1979)2009
A new look at the pathogenesis of asthma.
Review in Clinical science (London, England : 1979), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers, 1 of them a synthesis 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
67 citing papers in PubMed, 1 synthesis or guideline pooled it, 209 citations in OpenAlex.
- Breathing exercises for children with asthma.The Cochrane database of systematic reviews · 2016Pooled it
- Effects of altered airway function on exercise ventilation in asthmatic adults.Medicine and science in sports and exercise · 2014Trial
- Article
- Allergic sensitization and respiratory infection in infancy-Too early for two-hits on lung function?Pediatric allergy and immunology : official publication of the European Society of Pediatric Allergy and Immunology · 2026Article
- Effects of Eosinophilopoietins and C-C Chemokines on Chemotaxis, Adhesion, and ROS Production of Blood Eosinophil Subtypes in Asthma Patients.Journal of inflammation research · 2025Article
- Kiss1 receptor knockout exacerbates airway hyperresponsiveness and remodeling in a mouse model of allergic asthma.Respiratory research · 2024Article
- Impact of particulate air pollution on airway injury and epithelial plasticity; underlying mechanisms.Frontiers in immunology · 2024Review
- Mechanistic analysis of Th2-type inflammatory factors in asthma.Journal of thoracic disease · 2023Article
- Article
- Metal Allergy Mediates the Development of Oral Lichen Planus via TSLP-TSLPR Signaling.Journal of clinical medicine · 2022Article
- Allergic asthma manifestations in human and seropositivity toFrontiers in medicine · 2022Article
- Role of liver-X-receptors in airway remodeling in mice with chronic allergic asthma.Experimental and therapeutic medicine · 2021Article
- [Aryl hydrocarbon receptor modulates airway inflammation in mice with cockroach allergen-induced asthma by regulating Th17/Treg differentiation].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2021Article
- Extracellular Vesicles from Mesenchymal Stromal Cells for the Treatment of Inflammation-Related Conditions.International journal of molecular sciences · 2021Review
- Epithelial Barrier Dysfunction in Chronic Respiratory Diseases.Frontiers in physiology · 2021Review
- Airway Basal Cells, Protectors of Epithelial Walls in Health and Respiratory Diseases.Frontiers in allergy · 2021Review
- Evaluation of Human MSCs Treatment Frequency on Airway Inflammation in a Mouse Model of Acute Asthma.Journal of Korean medical science · 2020Article
- Aberrant cell migration contributes to defective airway epithelial repair in childhood wheeze.JCI insight · 2020Article
- Article
- Endomorphin-2- and Neurotensin- Based Chimeric Peptide Attenuates Airway Inflammation in Mouse Model of Nonallergic Asthma.International journal of molecular sciences · 2019Article
7 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
6 authors at 2 institutions in 1 country.
Funding
Abstract
Asthma is an inflammatory disorder of the conducting airways that has strong association with allergic sensitization. The disease is characterized by a polarized Th-2 (T-helper-2)-type T-cell response, but in general targeting this component of the disease with selective therapies has been disappointing and most therapy still relies on bronchodilators and corticosteroids rather than treating underlying disease mechanisms. With the disappointing outcomes of targeting individual Th-2 cytokines or manipulating T-cells, the time has come to re-evaluate the direction of research in this disease. A case is made that asthma has its origins in the airways themselves involving defective structural and functional behaviour of the epithelium in relation to environmental insults. Specifically, a defect in barrier function and an impaired innate immune response to viral infection may provide the substrate upon which allergic sensitization takes place. Once sensitized, the repeated allergen exposure will lead to disease persistence. These mechanisms could also be used to explain airway wall remodelling and the susceptibility of the asthmatic lung to exacerbations provoked by respiratory viruses, air pollution episodes and exposure to biologically active allergens. Variable activation of this epithelial-mesenchymal trophic unit could also lead to the emergence of different asthma phenotypes and a more targeted approach to the treatment of these. It also raises the possibility of developing treatments that increase the lung's resistance to the inhaled environment rather than concentrating all efforts on trying to suppress inflammation once it has become established.
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.