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Updated: Aug 12, 2026
08:26
Measuring the 50% Haemolytic Complement (CH50) Activity of Serum
Published on: March 29, 2010
Plasma complement C5 protects endothelial cells from polymorphonuclear neutrophil-derived, H2O2-mediated cytotoxicity
M Giroux1, D E Swartz, N V Christou
1LD MacLean Surgical Laboratories, McGill University Health Center, 687 Pine Avenue West, Montreal, Quebec H3A 1A1, Canada.
Surgical Infections
|February 21, 2003
Summary
Complement component C5 protects endothelial cells (EC) from damage caused by polymorphonuclear neutrophils (PMN) releasing hydrogen peroxide. This finding is crucial for understanding inflammatory responses and potential therapeutic targets.
Area of Science:
- Immunology
- Cell Biology
- Biochemistry
Background:
- Polymorphonuclear neutrophils (PMN) can damage endothelial cells (EC) via hydrogen peroxide release.
- This damage contributes to capillary leakage, multiple organ dysfunction syndrome, and high mortality.
- Plasma protects EC from PMN-mediated damage, suggesting protective factors exist in plasma.
Purpose of the Study:
- To investigate the role of plasma components in protecting endothelial cells (EC) from polymorphonuclear neutrophil (PMN)-mediated hydrogen peroxide damage.
- To identify specific complement components involved in this protective mechanism.
Main Methods:
- Human umbilical vein endothelial cells (EC) were cultured and coincubated with PMNs.
- Cytotoxicity was measured using gamma scintigraphy.
- Hydrogen peroxide (H2O2) levels and complement component C5 were quantified.
Main Results:
- Complement component C5, but not C3, conferred cytoprotection to EC, similar to whole serum.
- Removing C5 from serum significantly reduced EC protection against H2O2-mediated damage.
- Reintroducing C5 restored the protective effect, and C5 reduced H2O2-induced R-Phycoerythrin destruction.
Conclusions:
- Complement component C5 plays a significant role in protecting endothelial cells (EC) against hydrogen peroxide-mediated damage.
- This suggests C5 is a key mediator in the protective effects of plasma against PMN-induced EC injury.
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