Evidence for a Common Mechanism of Action of Interleukin‐1β, Tumor Necrosis Factor‐α, and Epidermal Growth Factor on Prostaglandin Production in Human Chorion Cells

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Abstract
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. 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. 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. 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.

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