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Platelet aggregation inhibition by mononuclear leukocytes
M A Schattner1, M R Finiasz, J A Notrica
1Departamentos de Hemostasia y Trombosis e Inmunología Academia Nacional de Medicina, Buenos Aires, Argentina.
Abstract:
In this study we have investigated the effect of human mononuclear leukocytes (ML) on platelet aggregation. The results obtained demonstrated that coincubation of platelets with nonstimulated ML decreased platelet aggregation induced by collagen or thrombin in a concentration-dependent manner. The inhibitory effect increased with the incubation period of the cells, reaching a plateau at 5 minutes. T and non-T enriched ML suspensions exerted an inhibitory effect similar to the total population of ML. Supernatants from ML or mixed cell suspensions also diminished platelet aggregation. 6-keto PGF1 alpha concentration in the supernatants was less than 10 pg/ml. Hemoglobin, L-arginine and cytochrome C did not modify the antiaggregating activity of ML, whereas superoxide dismutase potentiated the inhibition of aggregation mediated by ML. The inhibitory effect was not modified by monoclonal antibody (MoAb) against the lymphocyte function-associated antigen 1, alpha subunit (LFA-1 alpha) or by a MoAb directed against P-selectin. Our results demonstrated that ML inhibited platelet aggregation, at least partially, by the release of a soluble factor(s) distinct of prostacyclin or nitric oxide. Surface adhesion molecules seem also not to be involved.
Insights
Human mononuclear leukocytes (ML) inhibit platelet aggregation. This anti-aggregating effect is mediated by soluble factors, not surface molecules, and is potentiated by superoxide dismutase.
Area of Science:
- Immunology
- Hematology
- Cell Biology
Background:
- Platelet aggregation is crucial for hemostasis and thrombosis.
- Mononuclear leukocytes (ML) play roles in immune responses and may influence other cell types.
- The interaction between leukocytes and platelets is complex and not fully understood.
Purpose of the Study:
- To investigate the effect of human mononuclear leukocytes (ML) on platelet aggregation.
- To elucidate the mechanisms underlying ML-mediated modulation of platelet function.
- To identify soluble factors or cell surface molecules involved in this interaction.
Main Methods:
- Coincubation of human platelets with nonstimulated mononuclear leukocytes (ML).
- Induction of platelet aggregation using collagen or thrombin.
- Analysis of platelet aggregation in response to ML, ML supernatants, and various modulators.
- Assessment of soluble factors (e.g., 6-keto PGF1 alpha) and surface molecules (LFA-1 alpha, P-selectin) using specific antibodies.
Main Results:
- Nonstimulated ML significantly decreased collagen- or thrombin-induced platelet aggregation in a concentration-dependent manner.
- The inhibitory effect of ML on platelet aggregation increased with incubation time, plateauing at 5 minutes.
- Supernatants from ML also inhibited platelet aggregation, suggesting the release of soluble factors.
- Superoxide dismutase potentiated the anti-aggregating activity of ML, while other tested substances did not.
- Monoclonal antibodies against LFA-1 alpha and P-selectin did not affect the inhibitory activity.
Conclusions:
- Human mononuclear leukocytes (ML) possess anti-aggregating activity against platelets.
- This inhibition is mediated, at least partially, by soluble factors released by ML, distinct from prostacyclin or nitric oxide.
- Cell surface adhesion molecules like LFA-1 alpha and P-selectin do not appear to be involved in the ML-mediated inhibition of platelet aggregation.