Infection as an initiation of coagulation and inflammation: targeting the lung
Abstract number: S419
van der Poll T.
Patients with severe infections almost invariably show evidence of activation of the coagulation system. The lungs are amongst the most frequently affected organs during severe infection and sepsis. The abundant presence of intravascular and extravascular fibrin appears to be a specific hallmark of acute lung injury following sepsis and is much more obvious than the fibrin deposition in other organs. Tissue factor (TF) is regarded as the primary initiator of coagulation in severe infection. Effective blocking of the tissue factor pathway by either recombinant tissue factor pathway inhibitor (rTFPI) or anti-tissue factor antibodies in experimental sepsis attenuates lung injury and partially prevents pulmonary dysfunction. In addition, inhibition of tissue factor activity prevents local activation of coagulation in models of pneumonia. Another mechanism that contributes to fibrin deposition in the lung is the local depression of fibrinolysis, due to the increase of plasminogen activator inhibitor type I. These effects on pulmonary coagulation and fibrinolysis are regulated by various pro-inflammatory cytokines. This lecture will discuss the regulation and impact of pulmonary coagulation during severe infection.
|Session name:||18th European Congress of Clinical Microbiology and Infectious Diseases|
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