Fig. 2

A mechanism of DIC and MOF due to sepsis. When the pathogen-associated molecular patterns (PAMPs) (for example, endotoxin) and damage-associated molecular patterns (DAMPs) act on monocytes via TLR and on  neutrophils, a reactivated monocyte produce TF, various inflammatory cytokines, and HMGB1, and moreover, detection of PAMPs and DAMPs trigger neutrophil extracellular traps (NETs) release by neutrophils, promoting immunothrombosis. The uncontrolled immunothrombosis may lead to disseminated intravascular coagulation. And HMGB1 acts on EC and promotes upregulation of TF and downregulation of TM from EC, resulting endothelial cell injury, and microcirculation disorder develops DIC and MOF. TF tissue factor, TM thrombomodulin, TLR Toll-like receptor, IL-1β interleukin-1β, TNF-α tumor necrosis factor-α, EC endothelial cell, HMGB1 high-mobility group box protein 1, PAI plasminogen activator inhibitor, MOF multiple organ failure, NETs neutrophil extracellular traps