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Citation Information: J Clin Invest. 1980;66(3):406-414. https://doi.org/10.1172/JCI109870.
Abstract
We examined the role of prostaglandins and thromboxanes as mediators of plasma-dependent increased polymorphonuclear leukocyte adhesiveness induced by Escherichia coli lipopolysaccharide. The cyclo-oxygenase inhibitors—indomethacin and d,l-6-chloro-α-methyl-carbozole-2-acetic acid (R020-5720)—reduced lipopolysaccharide-induced adherence of polymorphonuclear leukocytes by 74 and 62%, respectively. In addition, inhibitors of thromboxane synthetase—imidazole, 9,11-azoprosta-5,13-dienoic acid, and 1-benzylimidazole—suppressed the stimulation of adherence by 31, 66, and 83%, respectively. Exogenous prostaglandins E1, E2, and F2α did not increase polymorphonuclear leukocyte adherence, nor were they detected in significant quantities in supernates of polymorphonuclear leukocytes exposed to lipopolysaccharide. However, inhibitors of both cyclo-oxygenase and thromboxane synthetase reduced increases in adherence induced by arachidonic acid (10 μg/ml), suggesting that lipopolysaccharide-mediated increases in adherence were due to an arachidonic acid product other than prostaglandin E2 or F2α. 8,11,14-Eicosatrienoic acid, a precursor of monoenoic prostaglandins, did not enhance polymorphonuclear leukocyte adhesiveness.
Authors
Philip J. Spagnuolo, Jerrold J. Ellner, Aviv Hassid, Michael J. Dunn
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