Evidence for a common mechanism of action of interleukin-1 beta, tumor necrosis factor-alpha, and epidermal growth factor on prostaglandin production in human chorion cells

Am J Reprod Immunol. 1993 Sep-Oct;30(2-3):146-53. doi: 10.1111/j.1600-0897.1993.tb00615.x.

Abstract

Problem: Although chorion produces prostaglandins in response to interleukin-1 beta (IL-1 beta), tumor necrosis factor alpha (TNF alpha), and epidermal growth factor (EGF), little attention has been given to the mechanisms of action of prostaglandin biosynthesis in this tissue.

Methods: IL-1 beta, TNF alpha, and EGF induced a concentration-related stimulation of prostaglandin E2 (PGE2) biosynthesis in human chorion cells, and this stimulation was enhanced by the addition of exogenous arachidonic acid.

Results: Protein synthesis inhibition with cycloheximide or actinomycin D resulted in complete abrogation of the stimulation of PGE2 production by IL-1 beta, TNF alpha, and EGF. Finally, all three stimulants induced a more rapid recovery of PGE2 production in chorion cells after acetylsalicylic acid pretreatment than controls.

Conclusions: It is suggested that IL-1 beta, TNF alpha, and EGF all act to stimulate human chorion PGE2 production primarily via induction of prostaglandin endoperoxide synthase activity.

MeSH terms

  • Aspirin / pharmacology
  • Cells, Cultured
  • Chorionic Villi / metabolism*
  • Cycloheximide / pharmacology
  • Cytokines / antagonists & inhibitors
  • Cytokines / physiology*
  • Dactinomycin / pharmacology
  • Dinoprostone / biosynthesis*
  • Epidermal Growth Factor / antagonists & inhibitors
  • Epidermal Growth Factor / physiology*
  • Female
  • Humans
  • Interleukin-1 / physiology
  • Pregnancy
  • Tumor Necrosis Factor-alpha / physiology

Substances

  • Cytokines
  • Interleukin-1
  • Tumor Necrosis Factor-alpha
  • Dactinomycin
  • Epidermal Growth Factor
  • Cycloheximide
  • Dinoprostone
  • Aspirin