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.
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.
Takaishi
O
O
Third Department of Internal Medicine and Department of Biosignal Analysis, Osaka City University Medical School, Osaka, Japan.
Arakawa
T
T
Fujiwara
Y
Y
Fukuda
T
T
Otani
K
K
Yamasaki
K
K
Higuchi
K
K
Kuroki
T
T
D015064:16,16-Dimethylprostaglandin E2 / Q000494:pharmacology*; D002470:Cell Survival; D002478:Cells, Cultured; D016480:Helicobacter pylori / Q000502:physiology*; D006801:Humans; D007375:Interleukin-1 / Q000096:biosynthesis* / Q000235:genetics; D009000:Monocytes / Q000378:metabolism*; D012333:RNA, Messenger / Q000032:analysis*; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors* / Q000235:genetics
D007375:Interleukin-1; D012333:RNA, Messenger; D014409:Tumor Necrosis Factor-alpha; D015064:16,16-Dimethylprostaglandin E2