Inflammation, innate immunity and blood coagulation

Journal: Hämostaseologie
ISSN: 0720-9355

Kongressausgabe 1. Joint Meeting GTH & NVTH: 54. Jahrestagung der Gesellschaft
für Thrombose- und Hämostase forschung e. V. & Symposium
van de Nederlandse Vereniging voor Trombose en Hemostase

Issue: Issues of 2010 (Vol. 30): Issue 1 2010 (1-50)
Pages: 5-9

Inflammation, innate immunity and blood coagulation

J. Xu (1), F. Lupu (1), C. T. Esmon (1, 2, 3)

(1) Cardiovascular Biology Research Program, Oklahoma Medical Research Foundation; (2) Howard Hughes Medical Institute; (3) Departments of Pathology and Biochemistry & Molecular Biology, University of Oklahoma Health Sciences Center, Oklahoma City, USA


thrombosis, inflammation, sepsis, multiorgan failure


Inflammation drives arterial, venous and microvascular thrombosis. Chronic inflammation contributes to arterial thrombotic complications, whereas acute inflammation drives venous thrombosis and microvascular thrombosis. Mechanistically, inflammation modulates thrombotic responses by upregulating procoagulants, downregulating anticoagulants and suppressing fibrinolysis. The inflammatory response can also result in cell apoptosis or necrosis. Products released from the dead cells, particularly histones, propagate further inflammation, tissue death and organ failure. Inhibition of histone mediated cytotoxicity appears to be a new mechanism for protecting against this deadly cascade.

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