Interleukin-6 acts in the fashion of a classical chemokine on monocytic cells by inducing integrin activation, cell adhesion, actin polymerization, chemotaxis, and transmigration

J Leukoc Biol. 2008 Dec;84(6):1521-9. doi: 10.1189/jlb.0308178. Epub 2008 Sep 2.

Abstract

Macrophages contribute to the innate immune response by eliminating bacteria, viral particles, and apoptotic bodies. They develop from circulating monocytes. In case of an infection, monocytes attach to the endothelial cells of the blood vessels, migrate along the endothelial cells, leave the circulatory system to enter the inflammatory tissue, and differentiate into macrophages. Cell migration is induced frequently by chemokines that act through G-protein-coupled receptors. Only a few cytokines signaling through single-transmembrane domain receptors have been shown to induce cell migration. Often, this potential depends on the induction of classical chemokines and is not a direct cellular effect. Here, we discovered IL-6 as a potent stimulant for monocytic cell migration. Furthermore, we present data about IL-6-induced integrin activation, cell attachment, actin polymerization, fibronectin-dependent migration, and transmigration through a layer of endothelial cells. Our results show that IL-6 fulfills all biological properties to mediate cell migration of monocytic cells, which may contribute to the proinflammatory potential of IL-6.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Actins / metabolism*
  • Animals
  • Blotting, Western
  • Cell Adhesion / drug effects*
  • Cell Movement / drug effects*
  • Cells, Cultured
  • Chemotaxis / drug effects*
  • Endothelium, Vascular / cytology
  • Endothelium, Vascular / metabolism
  • Humans
  • Integrins / metabolism*
  • Interleukin-6 / pharmacology*
  • Leukemia / metabolism
  • Leukemia / pathology
  • Macrophages / cytology
  • Macrophages / drug effects
  • Macrophages / metabolism
  • Monocytes / cytology
  • Monocytes / drug effects*
  • Monocytes / metabolism
  • Rats

Substances

  • Actins
  • Integrins
  • Interleukin-6