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Research Article Free access | 10.1172/JCI112693

Human platelet aggregation is initiated by peripheral blood mononuclear cells exposed to bacterial lipopolysaccharide in vitro.

B S Schwartz and M C Monroe

Find articles by Schwartz, B. in: PubMed | Google Scholar

Find articles by Monroe, M. in: PubMed | Google Scholar

Published November 1, 1986 - More info

Published in Volume 78, Issue 5 on November 1, 1986
J Clin Invest. 1986;78(5):1136–1141. https://doi.org/10.1172/JCI112693.
© 1986 The American Society for Clinical Investigation
Published November 1, 1986 - Version history
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Abstract

Platelet consumption is a prominent feature of disseminated intravascular coagulation. We investigated whether monocyte procoagulant activity (PCA) might play a role in platelet consumption associated with gram-negative septicemia. Human mononuclear cells exposed in vitro to lipopolysaccharide demonstrated parallel dose-dependent increases in PCA and ability to induce platelet aggregation. Induction of platelet aggregation required the generation of thrombin dependent on coagulation Factors VII, X, and II, and calcium. This is consistent with monocyte tissue factor initiating thrombin generation. A specific monoclonal antimonocyte antibody was used to identify monocytes via indirect immunofluorescence, and demonstrated that all monocytes were included in platelet aggregates. Mononuclear cells that did not express PCA did not induce platelet aggregation and monocytes were not surrounded by platelet clumps. These data suggest that monocytes induced to express tissue factor on their surface may be important mediators of endotoxin-induced platelet, as well as fibrinogen, consumption.

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