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|Title:||Release of Prostaglandins by Polymorphonuclear Leukocytes|
|Authors:||Wentzell, Robert Byron|
|Abstract:||<p>The release of prostaglandins from rat polymorphonuclear leukocytes obtained from peritoneal exudates was studied. Prostaglandin release by nonphagocytizing cells was stimulated by the presence of exogenous arachidonic acid and dihomo-ϒ-linolenic acid, the prostaglandin precursors. Prostaglandins synthesized from exogenous precursors were not stored intracellularly.</p> <p>Prostaglandin release was also stimulated during the phagocytosis of bacteria or zymosan particles in the absence of added precursor, although the quantities release were less than when exogenous precursor was present. The release of prostaglandins by phagocytizing cells showed many similarities to release of lysosomal enzymes, particularly those originating in the azurophil granules. Cells rendered incapable of ingesting particles by treatment with cytochalasin B released prostaglandins and lysosomal enzymes when presented with a phagocytic stimulus. Both prostaglandin and β-glucuronidase release from cytochalasin B-treated cells were inhibited by dibutyryl adenosine 3':5'-cyclic monophosphate and by colchicine.</p> <p>Resting cells treated with phorbol myristate acetate released lysozyme but did not release β-glucuronidase or prostaglandins. Both prostaglandins and lysosomal enzymes were released by the divalent cationic ionophore A23187 in the presence of Ca²⁺. Maximum prostaglandin release occurred at 1 μM A23187 whereas lysosomal enzyme release occurred in 2 stages with maxima at 1 μM and 5 μM A23187. In Ca²⁺-free buffer the respiratory burst which normally accompanies phagocytosis could be stimulated independently of prostaglandin and lysosomal enzyme release by the cationic ionophore X537A. The release of prostaglandins during phagocytosis and by A23187 was not due to activation of prostaglandin synthetase, but appeared to be due to increased availability of prostaglandin precursors.</p> <p>Preincubation of cells with exogenous prostaglandin precursors inhibited β-glucuronidase release when cells were subsequently exposed to a phagocytic stimulus. This effect was not due to prostaglandin biosynthesis but appeared to be a nonspecific fatty acid effect observed with other unsaturated fatty acids as well.</p>|
|Appears in Collections:||Open Access Dissertations and Theses|
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