Prostaglandin E(2) and tumour necrosis factor-alpha release by monocytes are modulated by phospholipids

Cytokine. 2000 Nov;12(11):1717-9. doi: 10.1006/cyto.2000.0762.

Abstract

The regulation of pro- and anti-mediator release from cells within the alveolar space would represent a desirable mechanism serving to protect this delicate gas-exchanging region of the lung. This study investigates the effect of alveolar surfactant lipids on the regulation of tumour necrosis factor alpha (TNF-alpha), a potent inflammatory cytokine, and prostaglandin E(2)(PGE(2)), a lipid mediator with anti-inflammatory properties. The results of this investigation reveal a marked effect on the release of these two important mediators from a monocytic cell line, MonoMac 6 (MM6), by phosphatidylcholine (PC), phosphatidylethanolamine (PE), cholesterol (Chol) and sphingomyelin (SM). PC, PE and Chol demonstrated marked downregulation of TNF-alpha production at lipid concentrations of 125 and 250 microg/ml. Interestingly, SM significantly up regulated the release of TNF-alpha at these concentrations. However, the release of PGE(2)in MM6 cells incubated with the same lipids was significantly increased with PC and Chol, and significantly decreased in cells pre-treated with SM. This indicates a role for these lipids in alveolar immunoregulation.

MeSH terms

  • Cell Line
  • Cell Survival
  • Cholesterol / pharmacology
  • Dinoprostone / metabolism*
  • Down-Regulation
  • Humans
  • Interferon-gamma / pharmacology
  • Lipid Metabolism
  • Lipopolysaccharides / pharmacology
  • Monocytes / metabolism*
  • Phosphatidylcholines / pharmacology
  • Phosphatidylethanolamines / pharmacology
  • Phospholipids / metabolism*
  • Sphingomyelins / pharmacology
  • Tumor Necrosis Factor-alpha / metabolism*

Substances

  • Lipopolysaccharides
  • Phosphatidylcholines
  • Phosphatidylethanolamines
  • Phospholipids
  • Sphingomyelins
  • Tumor Necrosis Factor-alpha
  • Interferon-gamma
  • Cholesterol
  • Dinoprostone