Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Experiment Videos

Eosinophil and airway nerve interactions.

P J Kingham1, Richard W Costello, W Graham McLean

  • 1Department of Pharmacology, University of Liverpool, Liverpool, UK.

Pulmonary Pharmacology & Therapeutics
|March 27, 2003
PubMed
Summary
This summary is machine-generated.

Related Concept Videos

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Digitally assessed home FEV<sub>1</sub> to identify the cause of poorly controlled asthma: a protocol paper for a prospective replicate cohort study.

BMJ open respiratory research·2025
Same author

Response to Biologics Along a Gradient of T2 Involvement in Patients With Severe Asthma: A Data-Driven Biomarker Clustering Approach.

The journal of allergy and clinical immunology. In practice·2025
Same author

Digital Assessment of Adherence to Asthma Inhalers in Primary Care, Is It Worth the Effort?

The journal of allergy and clinical immunology. In practice·2025
Same author

Prediction Pathway for Severe Asthma Exacerbations: A Bayesian Network Analysis.

Chest·2025
Same author

Impact of Biologics Initiation on Oral Corticosteroid Use in the International Severe Asthma Registry and the Optimum Patient Care Research Database: A Pooled Analysis of Real-World Data.

The journal of allergy and clinical immunology. In practice·2025
Same author

International Severe Asthma Registry (ISAR): 2017-2024 Status and Progress Update.

Tuberculosis and respiratory diseases·2025
Same journal

Effects of anumigilimab, an anti-G-CSF receptor mAb, after segmental LPS challenge: A Phase 1b trial in healthy volunteers.

Pulmonary pharmacology & therapeutics·2026
Same journal

Brain-derived neurotrophic factor (BDNF) signaling in respiratory disease: Mechanisms, neuroimmune crosstalk, and therapeutic implications.

Pulmonary pharmacology & therapeutics·2026
Same journal

PD05, a novel neutrophil elastase inhibitor, mitigates LPS-induced acute lung injury in a preclinical model.

Pulmonary pharmacology & therapeutics·2026
Same journal

The preclinical discovery and development of depemokimab for severe eosinophilic asthma.

Pulmonary pharmacology & therapeutics·2026
Same journal

TROP2 as a promising therapeutic target in lung cancer: Current clinical trial landscape and future directions.

Pulmonary pharmacology & therapeutics·2026
Same journal

Synergistic induction of apoptosis in lung cancer cells via TOP2A targeting through combined dihydroartemisinin and chrysin treatment.

Pulmonary pharmacology & therapeutics·2026
See all related articles

Eosinophils in asthma activate nerves by binding to adhesion molecules, causing increased acetylcholine release and loss of M(2) muscarinic receptor function in airway nerves.

Area of Science:

  • Immunology
  • Neuroscience
  • Respiratory Medicine

Background:

  • Eosinophils are found near airway nerves in asthma patients and animal models.
  • Nerve-eosinophil interactions alter cholinergic nerve and eosinophil function.

Purpose of the Study:

  • To investigate how eosinophil localization to airway nerves affects nerve function in asthma.
  • To elucidate the mechanism behind increased acetylcholine release in asthma.

Main Methods:

  • In vivo and in vitro studies examining nerve-eosinophil interactions.
  • Analysis of M(2) muscarinic receptor function and acetylcholine release.
  • Investigation of adhesion molecules involved in eosinophil-nerve binding.

Main Results:

Related Experiment Videos

  • Eosinophil activation and degranulation occur via specific adhesion molecules on nerves.
  • This interaction leads to M(2) muscarinic receptor dysfunction.
  • Loss of M(2) receptor function results in increased acetylcholine release from cholinergic nerves.

Conclusions:

  • Eosinophil interaction with airway nerves contributes to cholinergic dysfunction in asthma.
  • Adhesion molecule-mediated signaling is critical for this neuro-immune interaction.
  • Targeting these interactions may offer new therapeutic strategies for asthma.