Evidence map›Paper›PMID 26741046›Full record

ArticleAmerican journal of respiratory and critical care medicine2016

Neurophenotypes in Airway Diseases. Insights from Translational Cough Studies.

Maria G Belvisi, Mark A Birrell, Saifudin Khalid, Michael A Wortley, Rachel Dockry, Julie Coote, Kimberley Holt, Eric Dubuis, Angela Kelsall, Sarah A Maher and 3 more

Abstract read
In one paragraph

Article in American journal of respiratory and critical care medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
60citing papers in PubMed, 1 pooled it
11.5field-weighted citation impact, top 1% of its field
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

60 citing papers in PubMed, 1 synthesis or guideline pooled it, 124 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Trial
  4. Trial
  5. Trial
  6. Trial
  7. Review
  8. Review
  9. Asthma endotypes and theratypes.Chinese medical journal pulmonary and critical care medicine · 2026
    Review
  10. Research Progress on Upper Airway Cough Syndrome.World journal of otorhinolaryngology - head and neck surgery · 2025
    Review
  11. Article
  12. Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Update on the Role of β2AR and TRPV1 in Respiratory Diseases.International journal of molecular sciences · 2024
    Review
  20. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

13 authors at 3 institutions in 2 countries.

Maria G Belvisi1 Respiratory Pharmacology Group, Division of Airway Disease, National Heart and Lung Institute, Imperial College London, London, United Kingdom.ORCID 0000-0003-1652-4370
Mark A Birrell1 Respiratory Pharmacology Group, Division of Airway Disease, National Heart and Lung Institute, Imperial College London, London, United Kingdom.
Saifudin Khalid2 Centre for Respiratory and Allergy, University of Manchester, University Hospital of South Manchester, Manchester Academic Health Sciences Centre, Manchester, United Kingdom; and.
Michael A Wortley1 Respiratory Pharmacology Group, Division of Airway Disease, National Heart and Lung Institute, Imperial College London, London, United Kingdom.
Rachel Dockry2 Centre for Respiratory and Allergy, University of Manchester, University Hospital of South Manchester, Manchester Academic Health Sciences Centre, Manchester, United Kingdom; and.
Julie Coote1 Respiratory Pharmacology Group, Division of Airway Disease, National Heart and Lung Institute, Imperial College London, London, United Kingdom.
Kimberley Holt2 Centre for Respiratory and Allergy, University of Manchester, University Hospital of South Manchester, Manchester Academic Health Sciences Centre, Manchester, United Kingdom; and.
Eric Dubuis1 Respiratory Pharmacology Group, Division of Airway Disease, National Heart and Lung Institute, Imperial College London, London, United Kingdom.
Angela Kelsall2 Centre for Respiratory and Allergy, University of Manchester, University Hospital of South Manchester, Manchester Academic Health Sciences Centre, Manchester, United Kingdom; and.
Sarah A Maher1 Respiratory Pharmacology Group, Division of Airway Disease, National Heart and Lung Institute, Imperial College London, London, United Kingdom.
Sara Bonvini1 Respiratory Pharmacology Group, Division of Airway Disease, National Heart and Lung Institute, Imperial College London, London, United Kingdom.
Ashley Woodcock2 Centre for Respiratory and Allergy, University of Manchester, University Hospital of South Manchester, Manchester Academic Health Sciences Centre, Manchester, United Kingdom; and.
Jaclyn A Smith2 Centre for Respiratory and Allergy, University of Manchester, University Hospital of South Manchester, Manchester Academic Health Sciences Centre, Manchester, United Kingdom; and.ORCID 0000-0001-8837-4928
Manchester Academic Health Science Centre · GBImperial College London · GBLung Institute · US

Funding

Medical Research Council G0701918Medical Research Council MR/K020293/1
6 · The paper itself

Abstract

rationaleMost airway diseases, including chronic obstructive pulmonary disease (COPD), are associated with excessive coughing. The extent to which this may be a consequence of increased activation of vagal afferents by pathology in the airways (e.g., inflammatory mediators, excessive mucus) or an altered neuronal phenotype is unknown. Understanding whether respiratory diseases are associated with dysfunction of airway sensory nerves has the potential to identify novel therapeutic targets.

objectivesTo assess the changes in cough responses to a range of inhaled irritants in COPD and model these in animals to investigate the underlying mechanisms.

methodsCough responses to inhaled stimuli in patients with COPD, healthy smokers, refractory chronic cough, asthma, and healthy volunteers were assessed and compared with vagus/airway nerve and cough responses in a cigarette smoke (CS) exposure guinea pig model. MEASUREMENTS AND MAIN

resultsPatients with COPD had heightened cough responses to capsaicin but reduced responses to prostaglandin E2 compared with healthy volunteers. Furthermore, the different patient groups all exhibited different patterns of modulation of cough responses. Consistent with these findings, capsaicin caused a greater number of coughs in CS-exposed guinea pigs than in control animals; similar increased responses were observed in ex vivo vagus nerve and neuron cell bodies in the vagal ganglia. However, responses to prostaglandin E2 were decreased by CS exposure.

conclusionsCS exposure is capable of inducing responses consistent with phenotypic switching in airway sensory nerves comparable with the cough responses observed in patients with COPD. Moreover, the differing profiles of cough responses support the concept of disease-specific neurophenotypes in airway disease. Clinical trial registered with www.clinicaltrials.gov (NCT 01297790).

Indexed as

Administration, InhalationAdultAgedAnimalsCapsaicinCoughDinoprostoneDisease Models, AnimalFemaleGuinea PigsHumansMaleMiddle AgedPhenotypePulmonary Disease, Chronic ObstructiveRespiratory SystemCapsaicinDinoprostoneSmokeasthmaCOPDcoughguinea pigvagus nerve

Identifiers

PMID26741046
PMCPMC4910890
OpenAlexW2227501619

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.