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Research Article Free access | 10.1172/JCI107530

Hemolytic Plaque Formation by Leukocytes in Vitro CONTROL BY VASOACTIVE HORMONES

Kenneth L. Melmon, Henry R. Bourne, Yacob Weinstein, G. M. Shearer, Jerrold Kram, and Sara Bauminger

Division of Clinical Pharmacology, Department of Pharmacology, University of California Medical Center, San Francisco, California 94143

Division of Clinical Pharmacology, Department of Medicine, University of California Medical Center, San Francisco, California 94143

Department of Chemical Immunology, The Weizmann Institute of Science, Rehovot, Israel

Department of Biodynamics, The Weizmann Institute of Science, Rehovot, Israel

Find articles by Melmon, K. in: PubMed | Google Scholar

Division of Clinical Pharmacology, Department of Pharmacology, University of California Medical Center, San Francisco, California 94143

Division of Clinical Pharmacology, Department of Medicine, University of California Medical Center, San Francisco, California 94143

Department of Chemical Immunology, The Weizmann Institute of Science, Rehovot, Israel

Department of Biodynamics, The Weizmann Institute of Science, Rehovot, Israel

Find articles by Bourne, H. in: PubMed | Google Scholar

Division of Clinical Pharmacology, Department of Pharmacology, University of California Medical Center, San Francisco, California 94143

Division of Clinical Pharmacology, Department of Medicine, University of California Medical Center, San Francisco, California 94143

Department of Chemical Immunology, The Weizmann Institute of Science, Rehovot, Israel

Department of Biodynamics, The Weizmann Institute of Science, Rehovot, Israel

Find articles by Weinstein, Y. in: PubMed | Google Scholar

Division of Clinical Pharmacology, Department of Pharmacology, University of California Medical Center, San Francisco, California 94143

Division of Clinical Pharmacology, Department of Medicine, University of California Medical Center, San Francisco, California 94143

Department of Chemical Immunology, The Weizmann Institute of Science, Rehovot, Israel

Department of Biodynamics, The Weizmann Institute of Science, Rehovot, Israel

Find articles by Shearer, G. in: PubMed | Google Scholar

Division of Clinical Pharmacology, Department of Pharmacology, University of California Medical Center, San Francisco, California 94143

Division of Clinical Pharmacology, Department of Medicine, University of California Medical Center, San Francisco, California 94143

Department of Chemical Immunology, The Weizmann Institute of Science, Rehovot, Israel

Department of Biodynamics, The Weizmann Institute of Science, Rehovot, Israel

Find articles by Kram, J. in: PubMed | Google Scholar

Division of Clinical Pharmacology, Department of Pharmacology, University of California Medical Center, San Francisco, California 94143

Division of Clinical Pharmacology, Department of Medicine, University of California Medical Center, San Francisco, California 94143

Department of Chemical Immunology, The Weizmann Institute of Science, Rehovot, Israel

Department of Biodynamics, The Weizmann Institute of Science, Rehovot, Israel

Find articles by Bauminger, S. in: PubMed | Google Scholar

Published January 1, 1974 - More info

Published in Volume 53, Issue 1 on January 1, 1974
J Clin Invest. 1974;53(1):13–21. https://doi.org/10.1172/JCI107530.
© 1974 The American Society for Clinical Investigation
Published January 1, 1974 - Version history
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Abstract

Histamine, beta-adrenergic amines, and prostaglandins inhibited hemolytic plaque formation by splenic leukocytes from immunized mice. The same agents had previously been shown to prevent both the IgE-mediated release of histamine from human basophils and the immunologically specific cytolytic activity of murine lymphocytes, through stimulation of the production of cyclic AMP in leukocytes. We therefore tested the hypothesis that cyclic AMP might mediate an inhibitory effect of these drugs by comparing the ability of these agents to inhibit plaque formation with their effects on cyclic AMP accumulation in leukocytes. In splenic cells from three mouse strains, the dose-dependent effects of these agents of cyclic AMP correlated with their inhibition of plaque formation. Beta- but not alpha-adrenergic agonists were effective in both systems, and the effects of isoproterenol were inhibited by propranolol. Histamine was approximately equipotent with isoproterenol in both systems. Two prostaglandins (E1 and E2) were effective in both systems, but prostaglandin F2α was not. Dibutyryl cyclic AMP, a lipid-soluble analog of the endogenous nucleotide, inhibited plaque formation by cells of all three strains. Theophylline, an inhibitor of cyclic AMP degradation, inhibited plaque formation slightly, but potentiated the effects of histamine, isoproterenol, and the prostaglandins on both cyclic AMP accumulation and plaque formation. Finally, cholera enterotoxin, a potent activator of adenyl cyclase, produced a delayed inhibition of plaque formation and a parallel increase in leukocyte cyclic AMP content; both effects of the toxin were blocked by canine antitoxin. These results suggest that leukocyte cyclic AMP may act as a “second messenger” to suppress plaque formation in vitro. The inhibitory effects of hormones and cyclic AMP on plaque formation are strikingly similar to their effects on in vitro models of immediate and cell-mediated hypersensitivity. The physiologic significance of these findings is not yet known.

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