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Updated: May 6, 2026
Platelet Adhesion and Aggregation Under Flow using Microfluidic Flow Cells
Published on: October 27, 2009
Human platelet aggregation is initiated by peripheral blood mononuclear cells exposed to bacterial lipopolysaccharide
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.
Insights
Monocytes expressing procoagulant activity (PCA) can trigger platelet aggregation during gram-negative septicemia. This suggests monocytes are key mediators in endotoxin-induced consumption of platelets and fibrinogen.
Area of Science:
- Hematology
- Immunology
- Pathophysiology
Background:
- Disseminated intravascular coagulation (DIC) involves significant platelet consumption.
- Gram-negative septicemia is a common cause of DIC.
Purpose of the Study:
- To investigate the role of monocyte procoagulant activity (PCA) in platelet consumption during gram-negative septicemia.
- To determine if monocytes mediate endotoxin-induced platelet and fibrinogen consumption.
Main Methods:
- Human mononuclear cells were exposed to lipopolysaccharide (LPS) in vitro.
- Monocyte PCA and platelet aggregation were measured.
- Monocyte involvement in platelet aggregates was assessed using immunofluorescence.
Main Results:
- LPS exposure increased monocyte PCA and induced dose-dependent platelet aggregation.
- Thrombin generation, dependent on coagulation Factors VII, X, II, and calcium, was required for aggregation.
- Monocytes expressing PCA were identified within platelet aggregates, indicating their role in initiation.
Conclusions:
- Monocyte PCA, initiated by tissue factor expression, plays a significant role in platelet consumption during gram-negative septicemia.
- Monocytes are critical mediators of endotoxin-induced consumption of platelets and fibrinogen.
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