Figure 1.

Neutrophils induce blood coagulation during sepsis. Neutrophils accumulate and adhere to the vascular endothelium in collaboration with platelets during sepsis. There, they express tissue factor (TF), release TF-bearing neutrophil microparticles (NMPs), and expel neutrophil extracellular traps (NETs) that initiate the coagulation cascade. In addition, neutrophil-derived granule proteins, especially neutrophil elastase (NE), participate in thrombus formation by inhibiting tissue factor pathway inhibitor (TFPI) and anticoagulants such as antithrombin (AT) and activated protein C (APC). Both thrombi formation and endothelial damage lead to substantial microcirculatory damage and organ dysfunction if they occur systemically. RBC, red blood cell.