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The membrane attack complex of complement induces interleukin-8 and monocyte chemoattractant protein-1 secretion from

K S Kilgore1, C M Flory, B F Miller

  • 1Department of Pathology, University of Michigan Medical School, Ann Arbor, USA.

The American Journal of Pathology
|September 1, 1996
PubMed

Insights

The membrane attack complex (MAC) triggers human umbilical vein endothelial cells (HUVECs) to release neutrophil and monocyte chemokines. Interleukin-8 (IL-8) and MCP-1 are key chemokines involved in this complement-driven cell activation.

Area of Science:

  • Immunology
  • Cell Biology
  • Complement System

Background:

  • The membrane attack complex (MAC) is a key component of the complement system.
  • MAC assembly on cell surfaces can lead to cell lysis or activation.
  • Endothelial cell activation by MAC is relevant to inflammatory conditions like ischemia-reperfusion injury.

Purpose of the Study:

  • To investigate the capacity of sublytic MAC concentrations to induce chemokine secretion from human umbilical vein endothelial cells (HUVECs).
  • To identify the specific chemokines involved in MAC-induced endothelial cell activation.

Main Methods:

  • Exposure of HUVECs to sublytic concentrations of MAC.
  • Analysis of conditioned medium for chemotactic activities using enzyme-linked immunosorbent assays (ELISAs).
  • Northern hybridization to assess changes in chemokine mRNA levels.

Main Results:

  • Sublytic MAC assembly on HUVECs induced sequential secretion of neutrophil and monocyte chemotactic activities.
  • Neutrophil chemotaxis was primarily mediated by interleukin-8 (IL-8).
  • Monocyte chemotaxis was primarily mediated by MCP-1, with a later peak response.

Conclusions:

  • Sublytic MAC assembly on HUVECs triggers a sequential release of IL-8 and MCP-1.
  • This process leads to the recruitment of neutrophils and monocytes, contributing to inflammatory responses.
  • MAC-induced endothelial cell activation plays a role in complement-mediated inflammatory diseases.

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