Interleukin-1 (IL-1) has been reported to stimulate LH, GH, ACTH, and TSH release from cultured pituitary cells. IL-1 also has been found to be secreted in significant amounts by placental macrophages. To determine the possible role of IL-1 within the placenta, we studied the effects of human recombinant IL-1 on hCG release by long term cultures of human first trimester trophoblast and the JAR (human choriocarcinoma) cell line. IL-1 in concentrations ranging from 10(-11)-10(-9) mol/L stimulated hCG release from trophoblast cultures. This stimulatory effect was not mediated by prostaglandin E2 (PGE2), as indicated by the inability of indomethacin to block this stimulation as well as a lack of IL-1 effect on PGE2 release by trophoblast cells. At these doses, IL-1 exerted no effect on hCG release by JAR cells. PGE2, when used in high concentrations (10(-6)-10(-5) mol/L), stimulated the release of hCG by the trophoblasts as well as by the JAR cells. Neither IL-1 nor PGE2 stimulated the proliferation, [3H]thymidine incorporation, or differentiation (syncytium formation) of trophoblast or JAR cells. These results suggest that IL-1 may be an important local regulator of hCG secretion by first trimester trophoblasts.
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Yagel et al. (1989) studied this question.
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