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Alternative Complement Pathway Activation Provokes a Hypercoagulable State with Diminished Fibrinolysis.

Jason M Samuels1, Julia R Coleman1, Ernest E Moore2

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Shock (Augusta, Ga.)
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Activation of the alternative complement pathway triggers a hypercoagulable state. Complement component C3 influences fibrinolysis, and its inhibition enhances this process, while Cobra Venom Factor (CVF) reduces it.

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Area of Science:

  • Immunology
  • Hematology
  • Biochemistry

Background:

  • Prolonged activation of the alternative complement pathway is observed in various diseases.
  • The interplay between complement activation and hemostasis, particularly in platelets and neutrophils, is not fully understood.
  • This study investigates the impact of alternative complement pathway activation on human hemostatic potential.

Purpose of the Study:

  • To determine if alternative complement pathway activation leads to a hypercoagulable state.
  • To investigate the role of complement component C3 in regulating fibrinolysis.
  • To assess the effects of complement activation and inhibition on clot formation and strength.

Main Methods:

  • Alternative complement pathway activation was induced using Cobra Venom Factor (CVF) in whole blood.
  • Complement inhibition was achieved using Compstatin (C3/C3b inhibitor), SB290157 (C3a receptor inhibitor), and W54011 (C5a receptor inhibitor).
  • Coagulation parameters including reaction time, angle, maximum amplitude, and percent fibrinolysis (LY30) were measured using native thrombelastography.

Main Results:

  • Cobra Venom Factor (CVF) significantly increased clot strength (MA) and reduced fibrinolysis (LY30), indicating a hypercoagulable state.
  • Compstatin (C3/C3b inhibitor) did not affect clot formation or strength but dose-dependently increased fibrinolysis.
  • Inhibition of C3a and C5a receptors did not significantly alter coagulation parameters.

Conclusions:

  • Complement component C3 plays a role in regulating fibrinolysis; its inhibition enhances fibrinolysis, while CVF-mediated cleavage of C3 reduces it.
  • Alternative complement pathway activation, induced by CVF, promotes a hypercoagulable state characterized by increased clot strength.
  • C5a receptor inhibition partially reversed the effect of CVF on fibrinolysis.