Suppression of HMGB1 release by stearoyl lysophosphatidylcholine:an additional mechanism for its therapeutic effects in experimental sepsis

J Lipid Res. 2005 Apr;46(4):623-7. doi: 10.1194/jlr.C400018-JLR200. Epub 2005 Feb 1.

Abstract

Stearoyl lysophosphatidylcholine (LPC) has recently been proven protective against lethal sepsis by stimulating neutrophils to eliminate invading pathogens through an H2O2-dependent mechanism. Here, we demonstrate that stearoyl LPC, but not caproyl LPC, significantly attenuates circulating high-mobility group box 1 (HMGB1) levels in endotoxemia and sepsis by suppressing endotoxin-induced HMGB1 release from macrophages/monocytes. Neutralizing antibodies against G2A, a potential cell surface receptor for LPC, partially abrogated stearoyl LPC-mediated suppression of HMGB1 release. Thus, stearoyl LPC confers protection against lethal experimental sepsis partly by facilitating the elimination of the invading pathogens and partly by inhibiting endotoxin-induced release of a late proinflammatory cytokine, HMGB1.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Cells, Cultured
  • Disease Models, Animal
  • Endotoxins / pharmacology
  • HMGB1 Protein / metabolism*
  • Lysophosphatidylcholines / pharmacology*
  • Lysophosphatidylcholines / therapeutic use*
  • Macrophages / drug effects
  • Macrophages / metabolism
  • Male
  • Mice
  • Protein Transport
  • Sepsis / drug therapy*
  • Sepsis / metabolism*
  • Tumor Necrosis Factor-alpha / metabolism

Substances

  • Endotoxins
  • HMGB1 Protein
  • Lysophosphatidylcholines
  • Tumor Necrosis Factor-alpha
  • stearoyl alpha-lysolecithin