| ObjectiveSepsis is often associated with coagulation abnormalities. Interaction of activated platelets with leukocytes and proinflammatory cytokines are known to stimulate expression of tissue factor on leukocytes and consequently enhance coagulation activity. Previous studies have shown that TNF-a, IL-6and other proinflammatory cytokines were significantly elevated during endotoxemia in HSF1-knocked mouse. However, it was unclear that the knockout of HSF1could cause platelet activation, interaction of platelets and leukocyte and expression of tissue factor on leukocytes in mice during endotoxemia. In this study, HSF1-/-mice and HSF1+/+mice were recruited to explore the impact of the knocked HSF1on the activation of platelets and leukocytes, their interaction and the expression of tissue factor on leukocytes during the endotoxemia.MethodThe endotoxemia models were induced by intraperitoneal injection of endotoxin (8mg/kg) in HSF1-/-mice or HSF1+/+mice. The bleeding time was measured by the tail transection technique. The flow cytometric analyses were employed to detect platelet activation, platelet-leukocyte coaggregates and tissue factor (TF) expression on leukocytes.ResultsCompared with saline group, the bleeding time both in HSF1-/-mice or HSF+/+mice were markedly reduced, but significantly shorter in HSF1-/-mice than in HSF1+/+mice, showing enhanced clotting activity in HSF1-/-mice after endotoxemia.Compared with the saline group, the expression of P-selectin on platelet, percentage of platelet-leukocyte coaggregates and expression of tissue factor on leukocytes in HSF1-/-mice and HSF1+/+mice were enhanced during endotoxemia,but significantly higher in HSF1-/-mice than HSF1+/+mice.Conclusion①The clotting activity in HSF1-/-mice were enhanced during endotoxemia.②Platelet activation,interaction of platelets with leukocytes and expression of tissue factor on leukocytes were enhanced in HSF1-/-mice during endotoxemia. |
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