Evidence map›Paper›PMID 25049382›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2014

Population of sensory neurons essential for asthmatic hyperreactivity of inflamed airways.

Dimitri Tränkner, Nadeau Hahne, Ken Sugino, Mark A Hoon, Charles Zuker

Abstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 154 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
154citing papers in PubMed, 1 pooled it
–field-weighted citation impact
1 · What the graph read from 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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

154 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Trial
  3. Article
  4. The Role of the Nervous System in Lung Disease.Current neurology and neuroscience reports · 2026
    Review
  5. Review
  6. Review
  7. VipCell reports · 2026
    Article
  8. Vagal nerve TRPV3 regulates sedative-mediated appeasement.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Chemosensory tobacco product toxicology part 1: sensory mechanisms.Toxicological sciences : an official journal of the Society of Toxicology · 2025
    Review
  16. Chemosensory tobacco product toxicology part 2: toxicological testing, assays, and state of the science.Toxicological sciences : an official journal of the Society of Toxicology · 2025
    Review
  17. Article
  18. Article
  19. Neuro-immune cross-talk in cancer.Nature reviews. Cancer · 2025
    Review
  20. Article

94 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors.

Dimitri TränknerJanelia Farm Research Campus, Howard Hughes Medical Institute, Ashburn, VA 20147;
Nadeau HahneJanelia Farm Research Campus, Howard Hughes Medical Institute, Ashburn, VA 20147;
Ken SuginoJanelia Farm Research Campus, Howard Hughes Medical Institute, Ashburn, VA 20147;
Mark A HoonNational Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, MD 20892; and.
Charles ZukerJanelia Farm Research Campus, Howard Hughes Medical Institute, Ashburn, VA 20147;Department of Biochemistry and Molecular Biophysics,Department of Neuroscience, andHoward Hughes Medical Institute, Columbia College of Physicians and Surgeons, Columbia University, NY 10032 cz2195@columbia.edu.

Funding

Molecular Genetic Studies of SomatosensationZIADE000721 · NIDCR · NATIONAL INSTITUTE OF DENTAL & CRANIOFACIAL RESEARCH · PI HOON, MARK · 2009 to 2025
$26.6M
Howard Hughes Medical Institute
6 · The paper itself

Abstract

Asthma is a common debilitating inflammatory lung disease affecting over 200 million people worldwide. Here, we investigated neurogenic components involved in asthmatic-like attacks using the ovalbumin-sensitized murine model of the disease, and identified a specific population of neurons that are required for airway hyperreactivity. We show that ablating or genetically silencing these neurons abolished the hyperreactive broncho-constrictions, even in the presence of a fully developed lung inflammatory immune response. These neurons are found in the vagal ganglia and are characterized by the expression of the transient receptor potential vanilloid 1 (TRPV1) ion channel. However, the TRPV1 channel itself is not required for the asthmatic-like hyperreactive airway response. We also demonstrate that optogenetic stimulation of this population of TRP-expressing cells with channelrhodopsin dramatically exacerbates airway hyperreactivity of inflamed airways. Notably, these cells express the sphingosine-1-phosphate receptor 3 (S1PR3), and stimulation with a S1PR3 agonist efficiently induced broncho-constrictions, even in the absence of ovalbumin sensitization and inflammation. Our results show that the airway hyperreactivity phenotype can be physiologically dissociated from the immune component, and provide a platform for devising therapeutic approaches to asthma that target these pathways separately.

Indexed as

AnimalsAsthmaBronchial HyperreactivityGene DeletionGene SilencingMiceMice, Inbred C57BLPneumoniaReceptors, LysosphingolipidRespiratory SystemSensory Receptor CellsTRPV Cation ChannelsVagus NerveReceptors, LysosphingolipidTRPV1 protein, mouseTRPV Cation Channelsairway inflammationbronchospasms

Identifiers

PMID25049382
PMCPMC4128113

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.