The effect of inflammation on coagulation and vice versa.

Abstract

PURPOSE OF REVIEW:

In infection, inflammation is frequently accompanied by a disturbance of the normal hemostatic balance provided by procoagulant and anticoagulant mechanisms. This review summarizes recently acquired knowledge on the bimodal interactions between coagulation and inflammation in infection.

RECENT FINDINGS:

Infection elicits inflammation-induced coagulation via tissue factor. A net procoagulant state is further produced by impaired functioning of anticoagulant mechanisms among which is the protein C system. Protease activated receptors (PARs) form the molecular link between coagulation and inflammation. PAR1 mediates both detrimental (induced by thrombin) and protective (induced by activated protein C) cellular effects. Activated protein C protects against mortality in experimental endotoxemia and sepsis by effects that rely on PAR1, not on the anticoagulant properties of this protein.

SUMMARY:

Recent data provide new insights into how inflammation impacts on coagulation and vice versa, identifying crucial roles for PARs. This knowledge may assist in designing novel interventions targeted at the perpetuation of inflammation by mediators traditionally implicated in coagulation.

• Authors: Tom van der Poll, Johannes Daan de Boer, Marcel Levi
• Journal: Current opinion in infectious diseases (Curr Opin Infect Dis) Vol. 24 Issue 3 Pg. 273-8 (Jun 2011) ISSN: 1473-6527 [Electronic] United States
• PMID: 21330919 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Review)

Chemical References

• Receptors, Proteinase-Activated

Topics

• Blood Coagulation Disorders (physiopathology)
• Communicable Diseases (pathology)
• Humans
• Inflammation (physiopathology)
• Receptors, Proteinase-Activated (metabolism)