High-density lipoproteins attenuate interleukin-6 production in endothelial cells exposed to pro-inflammatory stimuli

Biochim Biophys Acta. 2005 Sep 15;1736(2):136-43. doi: 10.1016/j.bbalip.2005.08.003.

Abstract

The purpose of the present study was to investigate the ability of high-density lipoproteins (HDL) to attenuate endothelial dysfunction, by assessing down-regulation of cytokine-induced interleukin-6 (IL-6) production in cultured endothelial cells, and measuring plasma IL-6 levels in three groups of healthy individuals with low, average, or high plasma HDL-cholesterol. Human plasma HDL caused a concentration-dependent inhibition of TNFalpha-induced IL-6 production in human endothelial cells (by 58.5+/-1.5% at 2 mg of HDL-protein/ml). Reconstituted HDL made with apolipoprotein A-I (apoA-I) and phosphatidylcholine were as effective as plasma HDL, while lipid-free apoA-I or phosphatidylcholine liposomes had no effect. HDL attenuated IL-6 mRNA levels, an effect which occurs through inhibition of p38 MAP kinase. The median plasma IL-6 concentration was significantly higher in subjects with low HDL-cholesterol (2.54 pg/ml) compared with those with average or high HDL-cholesterol (1.31 pg/ml and 1.47 pg/ml, respectively). When all subjects were considered together, a lower HDL-cholesterol was the strongest independent predictor of higher IL-6 (F=25.38, P<0.001). By inhibiting IL-6 production and lowering plasma IL-6 concentration, HDL may limit the pro-atherogenic effects of both acute and chronic inflammatory states, of which IL-6 is a key orchestrator.

MeSH terms

  • Cells, Cultured
  • Down-Regulation
  • Endothelial Cells / drug effects
  • Endothelial Cells / immunology*
  • Endothelium, Vascular / cytology
  • Enzyme Activation
  • Humans
  • Interleukin-6 / blood*
  • Interleukin-6 / genetics
  • Lipoproteins, HDL / metabolism*
  • RNA, Messenger / metabolism
  • Tumor Necrosis Factor-alpha / pharmacology
  • p38 Mitogen-Activated Protein Kinases / metabolism

Substances

  • Interleukin-6
  • Lipoproteins, HDL
  • RNA, Messenger
  • Tumor Necrosis Factor-alpha
  • p38 Mitogen-Activated Protein Kinases