Considering its cytokine-dependent effects, the question then arises as to whether LPS can cause hypercoagulation by acting on the coagulation pathway more directly. One route is via tissue factor (TF) upregulation; TF is related to the cytokine receptor class II family, and is active early in the (extrinsic) coagulation cascade, where it is necessary to initiate thrombin formation from prothrombin . Recently, it was shown that LPS may upregulate TF; 100 ng ml−1 LPS added to healthy cord WB of newborns or the WB of healthy adults induced TF-mediated activation of haemostasis . LPS from Escherichia coli (100 ng ml−1) also activated the coagulation system when added to WB, via a complement- and CD14-dependent upregulation of TF, leading to prothrombin activation and hypercoagulation ; however, this was noted after 2 h, and therefore it was not an acute process . Note that in these studies, the anticoagulant was lepirudin, which prevents thrombin activation such that the effects of thrombin could not be evaluated. In this work, we used citrate as an anticoagulant.