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© Schattauer 2010


Inflammation, innate immunity and blood coagulation
J. Xu1; F. Lupu1; C. T. Esmon1,2,3

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

Thrombosis,inflammation, sepsis, multiorgan failure

Thrombose, Entzündung, Sepsis, Multiorganversagen

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 thromboticresponses 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 deadlycascade.

Entzündung fördert arterielle, venöse und mikrovaskuläre Thrombosen. Eine chronische Entzündung trägt zu arteriellen Thrombosekomplikationen bei, während eine akute Entzündung venöse und mikrovaskuläre Thrombosen fördert. Mechanistisch gesehen moduliert eine Entzündung die Thromboseantwort durch Hochregulierung von Prokoagulanzien, Herunterregulierung vonAntikoagulanzien und Unterdrückung der Fibrinolyse. Die Entzündungsreaktion kann auch zur Apoptose oder Nekrose von Zellen führen. Von abgestorbenen Zellen freigesetzte Produkte, vor allem Histone, fördern zusätzlich Entzündung, Gewebeuntergang und Organversagen. Eine Hemmung der histonvermittelten Zytotoxizität stellt anscheinend einen neuen Schutzmechanismus gegen diese tödliche Kaskade dar.Correspondence to: Dr. Charles Esmon Oklahoma Medical Research Foundation Howard Hughes Medical Institute 825 NE 13th Street Oklahoma City, OK 73104 USA Tel. 405/271 64 74, Fax 405/271 28 72 E-mail: esmonc@omrf.org

Entzündung, angeborene Immunität und Blutgerinnung Hämostaseologie 2010; 30: 5–9

There are links between inflammation and blood coagulation. ● On the arterial side, inflammation is clearlyassociated with the development of cardiovascular disease (6), but most of the studies are based on correlation rather than cause and effect. One very nice example of a cause and effect association indicating directly that inflammation contributes to cardiovascular disease was reported by Liu et al. (7)

where the investigators demonstrated that IL-6 polymorphisms that increase IL-6 levelswere associated with an increased risk for cardiovascular disease. On the venous side, one would anticipate that inflammation would also contribute to thrombotic disease. However, chronic low level inflammation that is associated with arterial thrombosis did not appear to be associated with venous thrombotic disease (12).

On the other hand, acute inflammation does contribute to venous thrombosisand pulmonary embolism (11). The latter findings are consistent with known changes that occur following an acute inflammatory response ( Fig. 1). Many of these changes are consistent with two of the three components of Virchow's triad, specifically increases in blood coagulability and changes in the vessel wall. In addition to the inflammatory cytokines like tumor necrosis factor and interleukin1, infection can trigger the release of neutrophil extracellular traps (NETs). These nets consist of DNA and nuclear proteins. The nets function to trap and clear pathogens from the circulation, reviewed in (8). While this is a beneficial immune function of the NETs, it comes at a cost – the NETs lead to vascular injury in vitro and liver damage in vivo (3). How the NETs cause tissue injury...
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