Evidence map›Paper›PMID 28587842›Full record

ReviewPulmonary pharmacology & therapeutics2017

Sustained sensitizing effects of tumor necrosis factor alpha on sensory nerves in lung and airways.

Ruei-Lung Lin, Qihai Gu, Mehdi Khosravi, Lu-Yuan Lee

Open access · greenAbstract readReview
In one paragraph

Review in Pulmonary pharmacology & therapeutics, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed, 1 pooled it
0.8field-weighted citation impact, top 25% 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

10 citing papers in PubMed, 1 synthesis or guideline pooled it, 15 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. Majie Cataplasm Promotes Th1 Response to Fight against Asthmatic Th2 Inflammation through NKs.Evidence-based complementary and alternative medicine : eCAM · 2022
    Article
  8. Article
  9. Review
  10. The voltage-gated sodium channel NaRespiratory physiology & neurobiology · 2019
    Article
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

4 authors at 2 institutions in 1 country.

Ruei-Lung LinDepartment of Physiology, University of Kentucky, Lexington, KY, USA.
Qihai GuDepartment of Biomedical Sciences, Mercer University, Macon, GA, USA.
Mehdi KhosraviDepartment of Medicine, University of Kentucky, Lexington, KY, USA.
Lu-Yuan LeeDepartment of Physiology, University of Kentucky, Lexington, KY, USA. Electronic address: lylee@uky.edu.
University of Kentucky · USMercer University · US

Funding

Kentucky Center for Clinical and Translational ScienceUL1TR001998 · NCATS · UNIVERSITY OF KENTUCKY · PI HARTMANN, KATHERINE E, KERN, PHILIP A · 2016 to 2025
$34.2M
Role of TRPV1 in asthma exacerbationU01AI123832 · NIAID · UNIVERSITY OF KENTUCKY · PI LEE, LU-YUAN · 2016 to 2018
$983k
Role of TRPV1 in Airway Hypersensitivity Induced by InflammationR01HL096914 · NHLBI · UNIVERSITY OF KENTUCKY · PI LEE, LU-YUAN · 2009 to 2010
$703k
NCATS NIH HHS UL1 TR001998NHLBI NIH HHS R01 HL096914NIAID NIH HHS U01 AI123832
6 · The paper itself

Abstract

Tumor necrosis factor alpha (TNFα) plays a significant role in the pathogenesis of airway inflammatory diseases. Inhalation of aerosolized TNFα induced airway hyperresponsiveness accompanied by airway inflammation in healthy human subjects, but the underlying mechanism is not fully understood. We recently reported a series of studies aimed to investigate if TNFα elevates the sensitivity of vagal bronchopulmonary sensory nerves in a mouse model; these studies are summarized in this mini-review. Our results showed that intratracheal instillation of TNFα induced pronounced airway inflammation 24 h later, as illustrated by infiltration of eosinophils and neutrophils and the release of inflammatory mediators and cytokines in the lung and airways. Accompanying these inflammatory reactions, the sensitivity of vagal pulmonary C-fibers and silent rapidly adapting receptors to capsaicin, a selective agonist of transient receptor potential vanilloid type 1 receptor, was markedly elevated after the TNFα treatment. A distinct increase in the sensitivity to capsaicin induced by TNFα was also observed in isolated pulmonary sensory neurons, suggesting that the sensitizing effect is mediated primarily through a direct action of TNFα on these neurons. Furthermore, the same TNFα treatment also induced a lingering (>7days) cough hyperresponsiveness to inhalation challenge of NH

Indexed as

AnimalsCoughDisease Models, AnimalHumansInflammationLungMiceReceptors, Tumor Necrosis FactorRespiratory HypersensitivitySensory Receptor CellsTumor Necrosis Factor-alphaVagus NerveReceptors, Tumor Necrosis FactorTumor Necrosis Factor-alphaAirway inflammationAsthmaCoughMouseTRPV1

Identifiers

PMID28587842
PMCPMC5701849
OpenAlexW2621194704

What OpenQuestion holds

Textmetadata
LicenceTDM
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.