Evidence map›Paper›PMID 19134001›Full record

ArticleBritish journal of pharmacology2009

Etanercept prevents airway hyperresponsiveness by protecting neuronal M2 muscarinic receptors in antigen-challenged guinea pigs.

Zhenying Nie, David B Jacoby, Allison D Fryer

Open access · bronzeAbstract read
In one paragraph

Article in British journal of pharmacology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.6field-weighted citation impact, top 18% 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

23 citing papers in PubMed, 39 citations in OpenAlex.

  1. Eosinophils prevent diet-induced airway hyperresponsiveness in mice on a high-fat diet.American journal of physiology. Lung cellular and molecular physiology · 2024
    Article
  2. Review
  3. Pioglitazone prevents obesity-related airway hyperreactivity and neuronal MAmerican journal of physiology. Lung cellular and molecular physiology · 2021
    Article
  4. Article
  5. Review
  6. Review
  7. Review
  8. Review
  9. Mechanisms of organophosphorus pesticide toxicity in the context of airway hyperreactivity and asthma.American journal of physiology. Lung cellular and molecular physiology · 2018
    Review
  10. Eosinophil and airway nerve interactions in asthma.Journal of leukocyte biology · 2018
    Review
  11. Article
  12. Newly divided eosinophils limit ozone-induced airway hyperreactivity in nonsensitized guinea pigs.American journal of physiology. Lung cellular and molecular physiology · 2017
    Article
  13. Protective Role of Eosinophils and TNFa after Ozone Inhalation.Research report (Health Effects Institute) · 2017
    Article
  14. Article
  15. Macrophage TNF-α mediates parathion-induced airway hyperreactivity in guinea pigs.American journal of physiology. Lung cellular and molecular physiology · 2013
    Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. Muscarinic receptor antagonists: effects on pulmonary function.Handbook of experimental pharmacology · 2012
    Review
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

3 authors at 1 institution in 1 country.

Zhenying NieDivision of Pulmonary and Critical Care Medicine, Oregon Health and Science University, Portland, OR 97239, USA.
David B Jacoby
Allison D Fryer
Oregon Health & Science University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

background and purposeIncreased tumour necrosis factor-alpha (TNF-alpha) is associated with airway hyperreactivity in antigen-challenged animals. In human asthmatics, TNF-alpha is increased and blocking it prevents airway hyperreactivity in some asthmatic patients. However, the mechanisms by which TNF-alpha mediates hyperreactivity are unknown. Airway hyperreactivity can be caused by dysfunction of neuronal M(2) muscarinic receptors that normally limit acetylcholine release from parasympathetic nerves. Here we test whether blocking TNF-alpha receptors with etanercept prevents M(2) receptor dysfunction and airway hyperreactivity in antigen-challenged guinea pigs. EXPERIMENTAL APPROACH: Ovalbumin-sensitized guinea pigs were challenged by inhalation of antigen. Some animals received etanercept (3 mg kg(-1) i.p.) 3 h before challenge. 24 h after challenge, airway hyperreactivity and M(2) receptor function were tested. Inflammatory cells in bronchoalveolar lavage, blood and lung were counted. TNF-alpha and its receptors were detected by real-time RT-PCR and immunocytochemistry in parasympathetic nerves from humans and guinea pigs and in human neuroblastoma cells. KEY

resultsAntigen-challenged animals were hyperreactive to vagal stimulation and neuronal M(2) receptors were dysfunctional. Both M(2) receptor dysfunction and airway hyperreactivity were prevented by etanercept. Etanercept reduced eosinophils around airway nerves, and in blood, bronchoalveolar lavage and airway smooth muscle. Also, TNF-alpha decreased M(2) receptor mRNA in human and guinea pig parasympathetic neurons. CONCLUSIONS AND IMPLICATIONS: Tumour necrosis factor-alpha may contribute to M(2) receptor dysfunction and airway hyperreactivity directly by decreasing receptor expression and indirectly by promoting recruitment of eosinophils, containing major basic protein, an M(2) antagonist. This suggests that etanercept may be beneficial in treatment of allergic asthma.

Indexed as

AnimalsAnti-Inflammatory Agents, Non-SteroidalBronchial HyperreactivityBronchoalveolar Lavage FluidBronchoconstrictionCell Line, TumorEosinophilsEtanerceptGuinea PigsHumansImmunoglobulin GMuscle, SmoothMyocardiumNeuronsOvalbuminParasympathetic Nervous SystemAnti-Inflammatory Agents, Non-SteroidalEtanerceptImmunoglobulin GOvalbuminReceptor, Muscarinic M2Receptors, Tumor Necrosis FactorTumor Necrosis Factor-alpha

Identifiers

PMID19134001
PMCPMC2697771
OpenAlexW2079242927

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.