Disseminated intracellular coagulation (DIC) is a serious, life-threatening disorder characterized by systemic activation of the blood coagulation pathway, which leads to generation and deposition of fibrin, resulting in microvascular thrombi in various organs and contributing to multiple organ dysfunction syndrome. Sepsis is frequently complicated by coagulopathy and, in about 35 % of severe cases, by DIC. The development and severity of DIC correlate with mortality in severe sepsis. We examined whether overt DIC is found in mice with cecal ligation and puncture (CLP)-induced sepsis, which serve as an animal model that has high clinical relevance to humans. We found that the number of blood platelets strikingly declined in CLP-induced septic mice as compared with sham-operated controls. Plasminogen activator inhibitor-1, a critical regulator of the fibrinolytic system, was markedly increased in all of major organs after CLP, and tissue factor, which has a pivotal role in initiating the extrinsic pathway of blood coagulation, was significantly elevated in lungs and kidneys after CLP. Finally, CLP mice exhibited an abnormal prothrombin time, suggesting that they represent an appropriate model for investigating sepsis-induced DIC.