Microparticles released by human neutrophils adhere to erythrocytes in the presence of complement

Exp Cell Res. 2005 Jul 15;307(2):381-7. doi: 10.1016/j.yexcr.2005.03.011. Epub 2005 Apr 22.

Abstract

The release of cell surface-derived microparticles, or ectosomes, has now been described for many different cell types. In various diseases characterized by systemic inflammation, the numbers of ectosomes released from specific cell-types are found increased manifold in the circulation. Their pro-inflammatory and pro-coagulant functions make them potentially important actors in disease establishment and/or progression. Until now, ectosomes have been believed to be free in the circulation. Herein, we provide evidence for sequestration of ectosomes derived from human polymorphonuclear neutrophils to erythrocytes, similarly to immune complexes. We show that ectosomes activate and bind complement in vitro. In whole blood, opsonization of ectosomes by complement mediated their immune adherence to erythrocytes through complement receptor 1. Taken together, our data suggest an important role for complement and erythrocytes in the sequestration, and possibly clearance, of blood-borne ectosomes stemming from neutrophils. The immune adherence described here may modify the biological activity and function of ectosomes.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Antigens, Neoplasm / analysis
  • Cell Adhesion Molecules / analysis
  • Complement Activation / drug effects
  • Complement C2 / metabolism
  • Complement C3 / metabolism
  • Complement Membrane Attack Complex / metabolism
  • Complement System Proteins / metabolism*
  • Cytoplasmic Vesicles / metabolism*
  • Cytoplasmic Vesicles / ultrastructure
  • Edetic Acid / pharmacology
  • Erythrocytes / metabolism*
  • Flow Cytometry
  • Humans
  • Microscopy, Electron, Transmission
  • Microscopy, Fluorescence
  • Neutrophils / chemistry
  • Neutrophils / metabolism*

Substances

  • Antigens, Neoplasm
  • Cell Adhesion Molecules
  • Complement C2
  • Complement C3
  • Complement Membrane Attack Complex
  • Complement System Proteins
  • Edetic Acid