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Infections and endothelial cells.

Tymen T Keller1, Albert T A Mairuhu, Martijn D de Kruif

  • 1Department of Vascular Medicine, Academic Medical Center, University of Amsterdam, Meibergdreef 9, 1105 AZ, Amsterdam, The Netherlands. t.t.keller@amc.uva.nl

Cardiovascular Research
|October 3, 2003
PubMed
Summary
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Systemic infections disrupt the endothelium, altering blood coagulation and fibrinolysis. The endothelium

Area of Science:

  • Vascular Biology
  • Hemostasis and Thrombosis
  • Infectious Disease Immunology

Background:

  • Systemic infections impact endothelial cells, influencing coagulation and fibrinolysis.
  • Endothelial dysfunction contributes to vasculitis and atherosclerosis.
  • The endothelium is central to regulating hemostasis.

Purpose of the Study:

  • To elucidate the endothelium's role in the interaction between inflammation and coagulation.
  • To understand how endothelial dysfunction leads to a procoagulant state.

Main Methods:

  • Review of literature on endothelial cell function in infection.
  • Analysis of molecular mechanisms of coagulation and fibrinolysis regulation by endothelium.
  • Examination of the interplay between inflammation, coagulation, and endothelial cells.

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Main Results:

  • Infection triggers endothelial changes, including tissue factor (TF) expression and impaired anticoagulant pathways (antithrombin III, TF pathway inhibitor (TFPI), protein C).
  • Dysfunctional endothelial cells lead to an imbalance in fibrinolysis due to altered plasminogen activator inhibitor (PAI) levels.
  • Increased soluble adhesion molecules and circulating endothelial cells signify endothelial damage.
  • Inflammation and coagulation exhibit significant bidirectional crosstalk, with the endothelium as a key mediator.

Conclusions:

  • The endothelium plays a critical role in mediating the complex interactions between systemic infections, inflammation, and hemostasis.
  • Endothelial dysfunction during infection promotes a procoagulant state, increasing the risk of thrombotic events.
  • Understanding this crosstalk is crucial for developing therapeutic strategies targeting infection-induced coagulopathy.