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Related Experiment Videos

Complement activation after oxidative stress: role of the lectin complement pathway.

C D Collard1, A Väkevä, M A Morrissey

  • 1Center for Experimental Therapeutics and Reperfusion Injury, Department of Anesthesiology, Perioperative and Pain Medicine, Brigham and Women's Hospital, Boston, Massachusetts 02115, USA.

The American Journal of Pathology
|May 4, 2000
PubMed
Summary

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The lectin complement pathway (LCP) activates complement after oxidative stress. Inhibiting mannose-binding lectin (MBL) may treat ischemia/reperfusion injury and other complement-mediated diseases.

Area of Science:

  • Immunology
  • Molecular Biology
  • Pathology

Background:

  • The complement system is crucial in tissue injury following oxidative stress.
  • The lectin complement pathway (LCP) and mannose-binding lectin (MBL) are implicated in this process.

Purpose of the Study:

  • To investigate the role of MBL and LCP in complement activation after endothelial oxidative stress.
  • To explore MBL inhibition as a potential therapeutic strategy.

Main Methods:

  • In vitro studies using human endothelial cells exposed to oxidative stress.
  • Experiments with MBL-deficient serum and anti-MBL monoclonal antibodies.
  • In vivo studies of rat myocardial reperfusion.

Main Results:

Related Experiment Videos

  • Oxidative stress induced endothelial iC3b deposition, which was inhibited by specific sugars and MBL deficiency.
  • Anti-MBL antibodies blocked MBL-dependent C3 deposition and reduced deposition after endothelial oxidative stress.
  • Increased C3 and MBL deposition was observed in ischemic tissues during rat myocardial reperfusion.

    • Conclusions:

    • The LCP mediates complement activation subsequent to tissue oxidative stress.
    • Inhibiting MBL presents a potential therapeutic avenue for ischemia/reperfusion injury and related conditions.