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Related Experiment Video

Updated: Jul 7, 2026

Rapid Magnetic-microbead Method for Efficient Purification of Low-density Neutrophils

Rapid Magnetic-microbead Method for Efficient Purification of Low-density Neutrophils

Published on: November 11, 2025

Complement activation by neutrophil granulocytes.

A E Asberg¹, T E Mollnes, V Videm

¹Department of Laboratory Medicine, Children's and Women's Health, Norwegian University of Science and Technology, Trondheim, Norway.

Scandinavian Journal of Immunology

|February 6, 2008

Summary

This summary is machine-generated.

Complement activation, crucial for immune defense, is minimally impacted by neutrophil fragmentation during cardiopulmonary bypass. Neutrophil-platelet interactions influence complement pathways, but complement activation is primarily upstream of neutrophil activation.

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Published on: November 4, 2022

Area of Science:

Immunology
Hematology
Cardiovascular Surgery

Background:

The complement system is vital for immune defense.
Cardiopulmonary bypass (CPB) triggers inflammatory responses involving complement, neutrophils, platelets, and endothelial cells.
The role of neutrophils, particularly fragmented ones, in complement activation during CPB is debated.

Purpose of the Study:

To investigate if intact or fragmented neutrophils activate the complement system.
To determine if neutrophil-platelet interactions affect complement activation during CPB.
To clarify the upstream or downstream role of complement activation relative to neutrophil activation in CPB.

Main Methods:

Incubation of lepirudin-anticoagulated plasma with resting, activated, or fragmented neutrophils, with or without platelets.
Assessment of complement activation by measuring specific markers (C1rs-C1 inhibitor complexes, C4bc, C3bBbP, C3bc, C5a, sC5b-9).

Main Results:

Significant complement activation was observed only with high doses of fragmented neutrophils or their supernatant, suggesting limited clinical relevance.
Unstimulated neutrophils induced C3 hydrolysis but were controlled by regulatory mechanisms.
Neutrophil-platelet interactions modulated complement activation, increasing classical and decreasing alternative pathways, similar to platelets alone.

Conclusions:

Neutrophil fragmentation during CPB has limited direct clinical significance for complement activation.
Complement activation is predominantly an upstream event to neutrophil activation within the inflammatory network during CPB.
Understanding these interactions is crucial for managing CPB-induced inflammation.