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

Adenosine, mast cells and asthma.

P Forsythe1, M Ennis

  • 1Department of Clinical Biochemistry, The Queen's University of Belfast, UK.

Inflammation Research : Official Journal of the European Histamine Research Society ... [Et Al.]
|August 12, 1999
PubMed
Summary

This review explores how adenosine interacts with mast cells in asthma. Adenosine is a natural substance that affects various cells, including mast cells, through specific receptors. Evidence suggests that adenosine may contribute to asthma by modulating mast cell activity and mediator release. However, the exact mechanism remains unclear due to the heterogeneity of mast cell responses and a lack of specific tools. The authors propose that BAL mast cells could serve as a relevant model for future studies. Understanding adenosine's role may lead to new treatment strategies for asthma.

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

Intrauterine Contraception Device Satisfaction and Continuation in an Urban Youth Clinic in British Columbia, Canada: A Longitudinal Survey Study.

Journal of obstetrics and gynaecology Canada : JOGC = Journal d'obstetrique et gynecologie du Canada : JOGC·2025
Same author

Amivantamab plus lazertinib versus osimertinib in first-line EGFR-mutant advanced non-small-cell lung cancer with biomarkers of high-risk disease: a secondary analysis from MARIPOSA.

Annals of oncology : official journal of the European Society for Medical Oncology·2024
Same author

Adult North Star Network (ANSN): Consensus Document for Therapists Working with Adults with Duchenne Muscular Dystrophy (DMD) - Therapy Guidelines.

Journal of neuromuscular diseases·2022
Same author

Colonoscopy skills improvement training improves patient comfort during colonoscopy.

Surgical endoscopy·2021
Same author

Differences in cecal microbiome of selected high and low feather-pecking laying hens.

Poultry science·2018
Same author

The modulatory effects of WE-14 on histamine release from rat peritoneal mast cells.

Inflammation research : official journal of the European Histamine Research Society ... [et al.]·2016

Area of Science:

  • Respiratory physiology within pulmonary medicine
  • Immunological mechanisms in allergic diseases
  • Pharmacological signaling pathways in asthma

Background:

Current understanding of asthma pathophysiology includes multiple interacting factors, yet the specific role of adenosine in modulating mast cell activity remains unclear. Prior research has shown that adenosine influences various cell types through adenosine receptors, but its precise contribution to asthma is not fully established. This gap motivated researchers to explore how adenosine interacts with mast cells, which are known to play a role in asthma. No prior work had resolved the heterogeneity of mast cell responses to adenosine. The complexity of adenosine receptor subtypes and their variable expression on mast cells adds to the uncertainty. This uncertainty drove the need to synthesize existing evidence on adenosine's effects in asthma. Researchers have already established that mast cells release mediators linked to asthma symptoms, but adenosine's role in this process is still debated. The lack of specific agonists and antagonists has limited progress in understanding these interactions.

Keywords:
Adenosine receptorsMast cell functionAsthma mechanismsBronchoconstriction

Frequently Asked Questions

Adenosine may modulate mast cell mediator release, which could contribute to asthma pathophysiology. This is proposed based on evidence from receptor subtype expression and bronchoconstrictive effects.

Adenosine receptors A1, A2a, A2b, and A3 are expressed on mast cells, but the pattern depends on the mast cell source.

The heterogeneity complicates interpretation of adenosine's effects, as responses vary depending on mast cell origin and receptor subtype expression.

BAL mast cells may provide an accurate model for studying adenosine/mast cell interactions in asthma.

Related Experiment Videos

Purpose Of The Study:

This review aimed to clarify the relationship between adenosine and mast cells in asthma by synthesizing current evidence. The specific problem addressed is the unclear mechanism by which adenosine modulates mast cell activity in this disease. The motivation stems from the need to understand how adenosine's effects on mast cells contribute to asthma pathophysiology. Researchers sought to examine whether adenosine's influence on mast cells could be a therapeutic target. The study focused on how adenosine receptors on mast cells might affect mediator release. The goal was to assess the potential of adenosine/mast cell interactions in asthma treatment. The review also aimed to identify limitations in current research methods. By analyzing receptor subtype expression and mediator modulation, the study aimed to provide a clearer picture of adenosine's role.

Main Methods:

The authors conducted a literature review to examine the interaction between adenosine and mast cells in asthma. They analyzed receptor subtype expression on mast cells, noting that the pattern depends on the mast cell source. The review included studies on adenosine's bronchoconstrictive effects and its modulation of mast cell mediators. Researchers evaluated evidence from in vitro and in vivo models to assess adenosine's influence. They also considered the heterogeneity of mast cell responses to adenosine. The review focused on how adenosine receptors (A1, A2a, A2b, A3) are expressed on mast cells. The authors examined the limitations of current pharmacological tools in studying these interactions. The final section of the review proposed BAL mast cells as a model for future investigations.

Main Results:

The strongest finding is that adenosine modulates mast cell mediator release, which may contribute to asthma pathophysiology. Adenosine receptors are expressed on mast cells, but the subtype pattern varies by cell source. Adenosine is a bronchoconstrictor and may exacerbate asthma symptoms. Evidence suggests that adenosine influences mast cell activity through receptor-mediated pathways. The exact mechanism of this interaction remains unclear due to receptor heterogeneity. Mast cell responses to adenosine are variable, complicating interpretation of results. The lack of specific agonists and antagonists has limited progress in this field. The review concludes that BAL mast cells may serve as a relevant model for future studies.

Conclusions:

The authors propose that adenosine's role in asthma is complex and involves modulation of mast cell activity. They suggest that adenosine may contribute to asthma through its effects on mast cell mediator release. The review highlights the need for better understanding of adenosine receptor subtypes on mast cells. The authors state that progress has been hampered by the heterogeneity of mast cell responses. They propose that BAL mast cells may provide a useful model for future investigations. The development of specific pharmacological tools is suggested to aid in understanding these interactions. The authors conclude that adenosine's role in asthma is not yet fully understood. A better understanding of adenosine's effects may lead to novel therapeutic approaches in asthma treatment.

A lack of highly specific adenosine receptor agonists and antagonists limits progress in understanding these interactions.

The authors suggest that a better understanding of adenosine's role may lead to novel therapeutic approaches in asthma treatment.