Reciprocal Modulation of Anti-IgE Induced Histamine Release from Human Mast Cells by A₁ and A(2B) Adenosine Receptors

Overview

Journal Br J Pharmacol

Publisher Wiley

Specialty Pharmacology

Date 2011 Apr 22

PMID 21506953

Citations 9

Authors

K H Yip

H Y A Lau

H Wise

Affiliations

Soon will be listed here.

Abstract

Background And Purpose: Adenosine is believed to participate in the pathological development of asthma through a mast cell-dependent mechanism. Our study aimed to pharmacologically characterize the functions of adenosine receptor (AR) subtypes (A₁, A(2A) , A(2B) and A₃) in primary human cultured mast cells (HCMC).

Experimental Approach: HCMC were derived from progenitor stem cells in buffy coat and the effects of adenosine receptor ligands on basal and IgE-dependent histamine release were evaluated.

Key Results: Adenosine and analogues alone did not induce HCMC degranulation. When HCMC were activated by anti-IgE after 10 min pre-incubation with adenosine, a biphasic effect on histamine release was observed with enhancement of HCMC activation at low concentrations of adenosine (10⁻⁹-10⁻⁷ mol·L⁻¹) and inhibition at higher concentrations (10⁻⁶-10⁻⁴ mol·L⁻¹). The potentiating action was mimicked by A₁ AR agonists CCPA and 2'MeCCPA, and inhibited by the A₁ AR antagonist PSB36. In contrast, the inhibitory action of adenosine was mimicked by the non-specific A₂ AR agonist CV1808 and attenuated by A(2B) AR antagonists PSB1115 and MRS1760. The non-selective AR antagonist CGS15943 attenuated both the potentiating and inhibitory actions.

Conclusions And Implications: We have defined for the first time the contribution of A₁ and A(2B) ARs, respectively, to the potentiating and inhibitory action of adenosine on human mast cell activation. With reference to the current trend of developing novel anti-asthmatic agents from AR ligands, our results suggest that inhibition of human mast cell activation would be a mechanism for A₁ AR antagonists, but not A(2B) AR antagonists.

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