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ATP enhances anti-IgE-induced hydrolysis of Pl-4,5,bisphosphate in cultivated human lung mast cells
Abstract   Peer reviewed

ATP enhances anti-IgE-induced hydrolysis of Pl-4,5,bisphosphate in cultivated human lung mast cells

Edward Stephen Schulman, Amir Pelleg, Li-Qing Jin, X Zhen and Eitan Friedman
Journal of allergy and clinical immunology, v 109(1 supplement 1), pp S322-S323
Jan 2002

Abstract

Extracellular adenosine 5'-triphosphate (ATP) has recently been identified as a novel pathophysiological mediator of obstructive airway diseases in general and asthma in particular. We have previously shown that ATP is the most potent and consistent enhancer of anti-IgE-induced histamine release from freshly isolated human lung mast cells (fHLMC) described to date. and that this effect is mediated by a G protein-coupled P2Y2 purinergic receptor (Am J Respir Cell Mol Bio120:530-7,1999). Recently, we have developed a novel experimental model that enables, for the first time, mature HLMC to survive, become homogeneous, proliferate and maintain remarkable functional integrity over weeks to months in culture. This new model, which provides large numbers of cultivated HLMC (cHLMC), was used to test the hypothesis that ATP enhances the FcERI-induced hydrolysis of PI-4. 5 bisphosphate (PIP2/ and thereby the production of inositol trisphosphate tIP3). Results (n=4): submaximal IgE receptor cross-linkage with the anti-FceRI monoclonal antibody 22E7 resulted in 17.9 --_ 8.2% histamine release. In the presence of ATP (10-4M), histamine release was enhanced to 39.5 _+ 12.2%. UTP (10-4M), an agonist at the P2Y2 receptor site. enhanced histamine release comparably to ATP. Neither ATP nor UTP alone triggered histamine release.

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Web of Science research areas
Allergy
Immunology
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