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IgE Receptor-Mediated Histamine Release in Human Lung Mast Cells: Modulation by Purinergic Receptor Ligands

Haruhisa Nishi1, Amir Pelleg2, Edward S Schulman2

  • 1Department of Pharmacology, The Jikei University School of Medicine, Tokyo, Japan harrywestjpjp@yahoo.co.jp.

Annals of Clinical and Laboratory Science
|September 22, 2016
PubMed
Abstract

Insights

Human lung mast cells (HLMCs) show purinergic receptor (P2YR) involvement in allergic histamine release. Adenosine and AMP-S compounds modulate histamine release, with AMP-S indicating functional P2YR activation that inhibits release.

Area of Science:

  • Immunology
  • Cell Biology
  • Pharmacology

Background:

  • Human lung mast cells (HLMCs) express G-protein coupled purinergic receptors (P2YR) and the homologous α-ketoglutarate receptor GPR99.
  • The specific role of P2YR in HLMCs regarding allergic responses remains unclear.
  • This study investigates the impact of purinergic and related compounds on histamine release (HR) from HLMCs.

Purpose of the Study:

  • To determine the effects of purinergic and purine-related compounds on allergic histamine release in HLMCs.
  • To investigate the expression of GPR99 following FcεRI-mediated allergic stimulation in HLMCs.

Main Methods:

  • Quantification of FcεRI-mediated histamine release (HR) in primary cultured HLMCs (cHLMC).
  • Assessment of GPR99 expression changes in response to FcεRI-mediated allergic stimulation.

Main Results:

  • Adenosine exhibited a dual effect on HR: enhancement at low concentrations and significant inhibition at high concentrations.
  • Adenosine 5'-monophosphate (AMP) did not influence FcεRI-mediated HR.
  • Adenosine-5'-O-thiomonophosphate (AMP-S), a non-hydrolysable AMP analog, demonstrated concentration-dependent inhibition of FcεRI-mediated HR without enhancement. High concentrations of α-ketoglutarate also moderately inhibited HR, but with distinct inhibitory characteristics compared to AMP-S.

Conclusions:

  • Primary cultured HLMCs express functional GPR99 receptors, which are upregulated after allergic stimulation.
  • The observed responsiveness to AMP-S provides the first evidence for functional P2YR expression in cHLMC.
  • Activation of P2YR in cHLMC can inhibit FcεRI-mediated histamine release, suggesting a role in modulating allergic responses.
Keywords:
FcεRIGPR99adenosineadenosine-5′-O-thiomonophosphatedegranulationhistamine releasehuman lung mast cellspurinergic receptors

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