ArticleProceedings of the National Academy of Sciences of the United States of America2009
A sensory neuronal ion channel essential for airway inflammation and hyperreactivity in asthma.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 226 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
226 citing papers in PubMed, 2 syntheses or guidelines pooled it, 456 citations in OpenAlex.
- Association between short-term ambient temperature variability (TV, DTR, and TCN) and asthma-related healthcare visit risk in children and adolescents: a systematic review and meta-analysis.Frontiers in public health · 2026Pooled it
- Global trends in research of neuroimmune in lung diseases over past decade: a bibliometric analysis.Frontiers in immunology · 2026Pooled it
- A TRPA1 inhibitor suppresses neurogenic inflammation and airway contraction for asthma treatment.The Journal of experimental medicine · 2021Trial
- Randomised placebo-controlled study of the effect of paracetamol on asthma severity in adults.BMJ open · 2014Trial
- TRPA1 Regulates Fibrosis-Associated Transcriptional Pathways in Human Lung Epithelial Cells.Basic & clinical pharmacology & toxicology · 2026Article
- Mechanisms and therapeutic strategies of asthma: from bench to bedside.Signal transduction and targeted therapy · 2026Review
- Sepsis-associated acute lung injury: do inflammatory lipid mediators flood the lungs by activating pulmonary TRP channels?Intensive care medicine experimental · 2026Review
- Neuroimmune Mechanisms in Equine Asthma: Primary Inflammatory Triggers, Neuroimmune Modulation and Chronic Airway Remodelling.Animals : an open access journal from MDPI · 2026Review
- VipCell reports · 2026Article
- Article
- Effects of Thermal Stress on Growth and Reproduction ofAnimals : an open access journal from MDPI · 2026Review
- Transient receptor potential ankyrin 1 promotes the expression of interferon-stimulated antiviral genes in human A549 lung epithelial cells.Molecular pharmacology · 2026Article
- Sleep disruption from inhalation of biomass smoke: a basis for coincident hypertension?Particle and fibre toxicology · 2025Article
- The role of TRPA1 in lung cancer.Translational lung cancer research · 2025Review
- Chemosensory tobacco product toxicology part 2: toxicological testing, assays, and state of the science.Toxicological sciences : an official journal of the Society of Toxicology · 2025Review
- Chemosensory tobacco product toxicology part 1: sensory mechanisms.Toxicological sciences : an official journal of the Society of Toxicology · 2025Review
- Ovalbumin-induced asthma leads to bone loss with Piezo channel suppression in mice.Communications biology · 2025Article
- Neuro-immune cross-talk in cancer.Nature reviews. Cancer · 2025Review
- Touching a Nerve: Neuroimmune Interactions in Asthma.Immunological reviews · 2025Review
- MrgprC11American journal of respiratory cell and molecular biology · 2025Article
166 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
15 authors at 2 institutions in 1 country.
Funding
Abstract
Asthma is an inflammatory disorder caused by airway exposures to allergens and chemical irritants. Studies focusing on immune, smooth muscle, and airway epithelial function revealed many aspects of the disease mechanism of asthma. However, the limited efficacies of immune-directed therapies suggest the involvement of additional mechanisms in asthmatic airway inflammation. TRPA1 is an irritant-sensing ion channel expressed in airway chemosensory nerves. TRPA1-activating stimuli such as cigarette smoke, chlorine, aldehydes, and scents are among the most prevalent triggers of asthma. Endogenous TRPA1 agonists, including reactive oxygen species and lipid peroxidation products, are potent drivers of allergen-induced airway inflammation in asthma. Here, we examined the role of TRPA1 in allergic asthma in the murine ovalbumin model. Strikingly, genetic ablation of TRPA1 inhibited allergen-induced leukocyte infiltration in the airways, reduced cytokine and mucus production, and almost completely abolished airway hyperreactivity to contractile stimuli. This phenotype is recapitulated by treatment of wild-type mice with HC-030031, a TRPA1 antagonist. HC-030031, when administered during airway allergen challenge, inhibited eosinophil infiltration and prevented the development of airway hyperreactivity. Trpa1(-/-) mice displayed deficiencies in chemically and allergen-induced neuropeptide release in the airways, providing a potential explanation for the impaired inflammatory response. Our data suggest that TRPA1 is a key integrator of interactions between the immune and nervous systems in the airways, driving asthmatic airway inflammation following inhaled allergen challenge. TRPA1 may represent a promising pharmacological target for the treatment of asthma and other allergic inflammatory conditions.
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.