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Updated: Aug 23, 2026

Isolation and Characterization of Neutrophil-derived Microparticles for Functional Studies
06:56

Isolation and Characterization of Neutrophil-derived Microparticles for Functional Studies

Published on: March 2, 2018

Activated polymorphonuclear neutrophils disseminate anti-inflammatory microparticles by ectocytosis

Olivier Gasser1, Jürg A Schifferli

  • 1Immunonephrology Laboratory, Department of Research, University Hospital Basel, Hebelstrasse 20, 4031 Basel, Switzerland. olivier.gasser@unibas.ch

Blood
|June 24, 2004
PubMed

Insights

Neutrophils release microparticles called ectosomes that reduce inflammation. These neutrophil ectosomes suppress inflammatory responses in macrophages, promoting the resolution of inflammation.

Area of Science:

  • Immunology
  • Cell Biology

Background:

  • Neutrophils release microparticles (ectosomes) upon activation.
  • Other microparticles modulate vascular homeostasis and coagulation.
  • Neutrophil ectosomes' role in inflammation is not fully understood.

Purpose of the Study:

  • To investigate the immunomodulatory effects of neutrophil ectosomes on macrophages.
  • To determine if neutrophil ectosomes possess pro- or anti-inflammatory properties.

Main Methods:

  • Human neutrophils were activated to release ectosomes.
  • Neutrophil ectosomes were applied to human macrophages.
  • Macrophage inflammatory cytokine release (IL-8, TNF-alpha) was measured.
  • Macrophage response to inflammatory stimuli (zymosan, LPS) was assessed.
  • TGF-beta1 release and phosphatidylserine exposure were analyzed.
  • Ectosome-cell contact necessity was tested using cytochalasin D.

Main Results:

  • Neutrophil ectosomes did not induce pro-inflammatory cytokine release (IL-8, TNF-alpha) in macrophages.
  • Neutrophil ectosomes increased transforming growth factor beta1 (TGF-beta1) release from macrophages.
  • Neutrophil ectosomes inhibited macrophage inflammatory responses to zymosan and LPS.
  • Both early TGF-beta1 secretion and surface phosphatidylserine on ectosomes contributed to the anti-inflammatory effect.
  • Direct ectosome-cell contact was sufficient for immunomodulation.

Conclusions:

  • Neutrophil-derived ectosomes act as potent anti-inflammatory effectors.
  • Ectosomes promote the resolution of inflammation by down-modulating macrophage activation.
  • These findings reveal a novel mechanism for early inflammatory control by neutrophils.

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