3.9 Article Proceedings Paper

Activated platelets enhance microparticle formation and platelet-leukocyte interaction in severe trauma and sepsis

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Publisher

LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/00005373-200105000-00005

Keywords

trauma; sepsis; SIRS; platelet; microparticle; platelet-leukocyte; interaction; P-selectin; endothelium

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Background: activated platelets have been recently reported to produce platelet microparticles and to enhance platelet-leukocyte interaction. The precise role of platelets in systemic inflammatory response syndrome (SIRS) has not been clarified. The objective of this study was to evaluate microparticle formation acid platelet-leukocyte interaction in severe trauma and sepsis. Methods: Twenty-six patients with severe SIRS (SIRS criteria and serum C-reactive protein > 10 mg/dL) and 12 healthy volunteers were studied. The severe SIRS was caused by trauma in 12 patients and sepsis in 14, Microparticle formation, P-selectin expression on platelets, platelet-monocyte binding, and platelet-polymorphonuclear leukocyte (PMNL) binding were measured by flow cytometry in the presence or absence of ionomycin, N-formyl-methionyl-leucyl-phenylalanine, or anti-CD62p monoclonal antibody. Soluble P-selectin, thrombomodulin, neopterin, and PMNL elastase in blood were also measured. Results: Microparticle formation, P-selectin expression on platelets, platelet-monocyte binding with or without ionomycin, and platelet-PMNL binding with ionomycin significantly increased in patients with severe SIRS in comparison with values in normal volunteers. The increased platelet-leukocyte binding in severe SIPS patients was markedly inhibited by P-selectin blockade and was not enhanced by N-formyl-methionyl-leucyl-phenylalanine, Soluble P-selectin, thrombomodulin, neopterin, and PMNL elastase in blood also increased in these patients. Conclusion: Activated platelets enhance microparticle formation and platelet-leukocyte interaction in severe trauma and sepsis, Enhanced platelet-leukocyte interaction is dependent on P-selectin expression and may be involved in the systemic inflammatory response after severe inflammatory insult.

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