Metabolic response of macrophages to injury promoted by the activated complement system

Cell Biochem Funct. 1999 Sep;17(3):175-82. doi: 10.1002/(SICI)1099-0844(199909)17:3<175::AID-CBF825>3.0.CO;2-S.

Abstract

In nucleated cells, the swelling promoted by a complement system (CS) attack is not enough to promote cell death, because unlike erythrocytes these cells are able to eliminate cytolytic complement channels from the plasma membrane, by processes that include endocytosis. Several studies have demonstrated that the resistance of nucleated cells to the injury promoted by the CS is related to the cellular metabolism. Despite this, to the present day, no study has clearly related cell survival capacity to injury by the CS to its energetic metabolic status. In macrophages, the challenge imposed by the CS provoked an increase in the total amount of glucose incorporated into fatty acids, including phospholipids and cholesterol; substrates for membrane synthesis. The inhibition of cholesterol synthesis promoted an increase of the cell death rate. These data support the importance of cholesterol metabolism for macrophage resistance to necrosis induced by the activated complement system.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Acetates / metabolism
  • Animals
  • Cell Death
  • Cells, Cultured
  • Cholesterol / metabolism
  • Cholesterol Esters / metabolism
  • Complement Activation
  • Complement System Proteins / immunology*
  • Glucose / metabolism
  • Glutamine / metabolism
  • Macrophages, Peritoneal / cytology
  • Macrophages, Peritoneal / immunology
  • Macrophages, Peritoneal / metabolism*
  • Male
  • Mevalonic Acid / metabolism
  • Phospholipids / metabolism
  • Pyruvic Acid / metabolism
  • Rats
  • Rats, Wistar

Substances

  • Acetates
  • Cholesterol Esters
  • Phospholipids
  • Glutamine
  • Pyruvic Acid
  • Complement System Proteins
  • Cholesterol
  • Glucose
  • Mevalonic Acid