OBJECTIVE:
The purpose of this study was to determine the mechanism of action of the cytokines tumor necrosis factor-α (TNFα) and interleukin-1β (IL-1β) on the stimulation of prostaglandin (PG) production in human decidua.
METHODS:
Decidual cells from term placentas were grown in culture until confluent. Incuba tions were performed with TNFα or IL-1β, and with cycloheximide, actinomycin D, arachidonic acid, or acetylsalicylic acid (ASA). Prostaglandin E2 was measured by radioimmunoassay and cellular protein determined.
RESULTS:
The concentration-related stimulation of decidual PGE2 production by IL-1β and TNFα was completely abrogated by cycloheximide and actinomycin D treatment. Although arachidonic acid alone stimulated decidual PGE2 biosynthesis, the addition of IL-1β or TNFα consistently augmented this effect. Both cytokines induced recovery of PGE2 biosynthesis from ASA pretreatment more rapidly than controls.
CONCLUSIONS:
Interleukin-1β and TNFα both act on decidual PG biosynthesis in a manner requiring new protein synthesis. In combination with our other results, this suggests that IL-1β and TNFα act to induce PG endoperoxide synthase activity. (J Soc Gynecol Invest 1994;1: 31-6)