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Table 2 The inflammatory effects of coagulation and loss of anticoagulants

From: Bench-to-bedside review: Functional relationships between coagulation and the innate immune response and their respective roles in the pathogenesis of sepsis

Coagulation parameter

Proinflammatory Effects

Thrombin generation

Promotes cytokine and chemokine synthesis (IL-6, IL-8) via PARs, P-selectin, E-selectin and PAF expression, which facilitates neutrophil–endothelial cell interactions, bradykinin and histamine release

Factor Xa and TF–factor VIIa complex generation

Promotes cytokine and chemokine synthesis (IL-6, IL-8) via PAR-1 and PAR-2

Reduced antithrombin

Results in the loss of prostacyclin synthesis by endothelial cells, increased cytokine synthesis, increased leukocyte adherence and chemotaxis

Reduced protein C/protein S activity

Results in increased E-selectin expression, increased cytokine generation and neutrophil adherence; promotes apoptosis of endothelial cells

Reduced TFPI activity

Results in loss of regulation of cytokine synthesis within microcirculation

Platelet activation

Platelet derived P-selectin promotes neutrophil adherence, neutrophil–endothelial cell interactions; platelet CD40 ligand promotes endothelial cell chemokine and adhesion molecule expression; activated platelets secrete chemokines and IL-1β

Intravascular fibrin deposition

Neutrophil and monocyte adherence

Reduced thrombomodulin expression on endothelial cells

Loss of TM lectin domain activity that inhibits neutrophil–endothelial cell adherence may promote neutrophil binding

  1. IL, interleukin; PAF, platelet-activating factor; PAR, protease activated receptor; TF, tissue factor; TFPI, tissue factor pathway inhibitor; TM, thrombomodulin.