Hamostaseologie 2010; 30(01): 5-9
DOI: 10.1055/s-0037-1617146
Review
Schattauer GmbH

Inflammation, innate immunity and blood coagulation

Entzündung, angeborene Immunität und Blutgerinnung
J. Xu
1   Cardiovascular Biology Research Program, Oklahoma Medical Research Foundation
,
F. Lupu
1   Cardiovascular Biology Research Program, Oklahoma Medical Research Foundation
,
C. T. Esmon
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
› Author Affiliations
Further Information

Publication History





Publication Date:
29 December 2017 (online)

Summary

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.

Zusammenfassung

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 von Antikoagulanzien und Unterdrückung der Fibrinolyse. Die Entzündungsreaktion kann auch zur Apoptose oder Nekrose von Zellen führen. Von abge -storbenen Zellen freigesetzte Produkte, vor allem Histone, fördern zusätzlich Entzündung, Gewebeuntergang und Organversagen. Eine Hemmung der histonvermittelten Zyto -toxizität stellt anscheinend einen neuen Schutzmechanismus gegen diese tödliche Kaskade dar.

 
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