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Am J Physiol Lung Cell Mol Physiol 281: L844-L851, 2001;
1040-0605/01 $5.00
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Vol. 281, Issue 4, L844-L851, October 2001

Regulation of eosinophil function by phosphatidylinositol-specific PLC and cytosolic PLA2

Akiko Sano1, Xiangdong Zhu1, Hiroyuki Sano1, Nilda M. Muñoz1, Evan Boetticher1, and Alan R. Leff1,2

1 Section of Pulmonary and Critical Care Medicine, Department of Medicine, and 2 Departments of Neurobiology, Pharmacology, Physiology, and Critical Care and Committees on Clinical Pharmacology and Cell Physiology, Division of the Biological Sciences, The University of Chicago, Chicago, Illinois 60637

We examined the regulatory role of cytosolic phospholipase A2 (cPLA2) and phosphatidylinositol (PI)-specific phospholipase C (PLC) in the degranulation of human eosinophils and leukotriene (LT) C4 synthesis. Activation with formyl-Met-Leu-Phe + cytochalasin B (fMLP/B) caused a time-dependent release of eosinophil peroxidase (EPO) and LTC4, which was inhibited by pertussis toxin. By immunoblotting, eosinophil PLC-beta 2 and -gamma 2 isoforms were identified, and PLC activation was measured as a function of inositol 1,4,5-trisphosphate concentration. Stimulated release of EPO and intracellular Ca2+ concentration was inhibited by ET-18-OCH3, a PI-PLC inhibitor, whereas trifluoromethylketone (TFMK), a cPLA2 blocker, had no inhibitory effect. Both TFMK and ET-18-OCH3 attenuated stimulated arachidonate release and LTC4 secretion, suggesting that activation of both PLC and cPLA2 is essential for LTC4 synthesis caused by fMLP/B. The structurally unrelated protein kinase C inhibitors bisindolylmaleimide, Ro-31-8220, and Go-6976 all blocked fMLP/B-induced EPO release but not LTC4 secretion. 1,2-bis(2-Aminophenoxy)ethane-N,N,N',N'- tetraacetic acid acetoxymethyl ester, an intracellular Ca2+ chelator, suppressed both EPO release and LTC4 secretion. We found that fMLP/B-induced LTC4 secretion from human eosinophils is regulated by PI-PLC through calcium-mediated activation of cPLA2. However, cPLA2 does not regulate eosinophil degranulation.

arachidonate; protein kinase C; calcium concentration; phospholipase C isoforms


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