Inhibition by 16,16-dimethyl prostaglandin E2 of tumor necrosis factor-alpha and interleukin-1beta production and messenger RNA expression in human monocytes stimulated by Helicobacter pylori

Dig Dis Sci. 1999 Dec;44(12):2405-11. doi: 10.1023/a:1026614400820.

Abstract

We investigated the effects of 16,16-dimethyl prostaglandin E2 on the production of tumor necrosis factor-alpha and interleukin-1beta in human monocytes stimulated with Helicobacter pylori. Monocytes isolated from human peripheral blood were incubated for 24 hr with the extract of H. pylori diluted 1:100 to 1:100,000 by volume, a combination of the extract and 16,16-dimethyl prostaglandin E2, or a vehicle alone. The extract stimulated the production of tumor necrosis factor-alpha and interleukin-1beta and the expression of their messenger RNA in a dose-dependent manner. 16,16-Dimethyl prostaglandin E2 inhibited the production of these cytokines and their messenger RNA in the presence of H. pylori at doses higher than 10(-6) M, predominantly with tumor necrosis factor-alpha. These data suggest that antiinflammatory effects of prostaglandins on gastric mucosa are in part related to their effects on inhibition of production of proinflammatory cytokines by monocytes.

MeSH terms

  • 16,16-Dimethylprostaglandin E2 / pharmacology*
  • Cell Survival
  • Cells, Cultured
  • Helicobacter pylori / physiology*
  • Humans
  • Interleukin-1 / biosynthesis*
  • Interleukin-1 / genetics
  • Monocytes / metabolism*
  • RNA, Messenger / analysis*
  • Tumor Necrosis Factor-alpha / antagonists & inhibitors*
  • Tumor Necrosis Factor-alpha / genetics

Substances

  • Interleukin-1
  • RNA, Messenger
  • Tumor Necrosis Factor-alpha
  • 16,16-Dimethylprostaglandin E2