The interactions between inflammation and coagulation

Summary Inflammation initiates clotting, decreases the activity of natural anticoagulant mechanisms and impairs the fibrinolytic system. Inflammatory cytokines are the major mediators involved in coagulation activation. The natural anticoagulants function to dampen elevation of cytokine levels. Furt...

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Veröffentlicht in:British journal of haematology Jg. 131; H. 4; S. 417 - 430
1. Verfasser: Esmon, Charles T.
Format: Journal Article
Sprache:Englisch
Veröffentlicht: Oxford, UK Blackwell Science Ltd 01.11.2005
Blackwell
Schlagworte:
Apoptosis
Biological and medical sciences
Blood Coagulation
Fibrinolysis - physiology
Hematologic and hematopoietic diseases
Humans
inflammation
Inflammation - blood
Inflammation - complications
Inflammation - pathology
Inflammation Mediators - blood
Medical sciences
protein C pathway
sepsis
thrombosis
Thrombosis - etiology
vascular biology
Blood coagulation
Hematology
Cardiovascular disease
Protein C
Biology
Inflammation
vascular biology
Thrombosis
Infection
Vascular disease
Sepsis syndrome
Blood vessel
Circulatory system
protein C pathway
sepsis
ISSN:0007-1048, 1365-2141
Online-Zugang:Volltext
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Zusammenfassung:Summary Inflammation initiates clotting, decreases the activity of natural anticoagulant mechanisms and impairs the fibrinolytic system. Inflammatory cytokines are the major mediators involved in coagulation activation. The natural anticoagulants function to dampen elevation of cytokine levels. Furthermore, components of the natural anticoagulant cascades, like thrombomodulin, minimise endothelial cell dysfunction by rendering the cells less responsive to inflammatory mediators, facilitate the neutralisation of some inflammatory mediators and decrease loss of endothelial barrier function. Hence, downregulation of anticoagulant pathways not only promotes thrombosis but also amplifies the inflammatory process. When the inflammation–coagulation interactions overwhelm the natural defence systems, catastrophic events occur, such as manifested in severe sepsis or inflammatory bowel disease.
Bibliographie:ObjectType-Article-1
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ObjectType-Review-3
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ISSN:0007-1048
1365-2141
DOI:10.1111/j.1365-2141.2005.05753.x