Source: Annual Congress 2001 - Molecular and cellular pathology of asthma
Disease area: Airway diseases

Abstract

Background: Adenosine can modulate many physiological processes and evidence suggests that it contributes to asthma pathophysiology. Adenosine has previously been shown to modulate anti-IgE induced histamine release from human basophils. The aim of this work was to investigate the adenosine receptor(s) mediating these effects.
Methods: Basophils from healthy volunteers were challenged with anti-IgE in the presence of adenosine (10-8-10-4M), CGS21680 (10-8-10-4M), CPA (10-8-10-4M) or IB-MECA (10-8-10-5M). Adenosine or its agonists were administered 15 min prior to challenge, at the same time as the challenge or 15 min post challenge. Histamine release was determined by an automated fluorimetric assay.
Results: Adenosine and its agonists dose-dependently inhibited anti-IgE-induced histamine release when the cells were pre-incubated with the nucleosides before challenge with anti-IgE (maximum inhibition: adenosine: 40.8±]3.4%; CGS21680: 27±]2.5%; CPA: 24.6±]7.5%; IB-MECA: 30.4±]2.4%). Inhibition was also seen after simultaneous addition of the agents (maximum inhibition: adenosine: 26.6±]3.9%, CGS21680: 18.3±]6.2%; CPA: 21.1±]10.3%, IB-MECA: 23.4±]7%). Even adding the agents 15 min after the stimulus elicited some inhibition (maximum inhibition; adenosine: 12.7±]3.5%, CGS21680: 20.9±]12.3%, CPA: 14.2±]3%, IB-MECA: 10.8±]4.6%).
Conclusions: Adenosine and its agonists inhibited anti-IgE-induced histamine release from human basophils in a receptor mediated, concentration-dependent manner. The degree of inhibition depended on the time of incubation with the agents. However, in contrast to previous work, we did not observe potentiation of response when adenosine or its agonists were administered after the challenge.


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Citations should be made in the following way:
M. Livingston, L. G. Heaney, M. Ennis (Belfast, Ireland). Inhibition of basophil activation by adenosine and its agonists. Eur Respir J 2001; 16: Suppl. 31, 3568

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