The mechanism of the onset of labor, though one of the essential features of the human reproductive physiology, has not been fully elucidated. It is widely accepted that prostaglandin (PG) plays an important role in human parturition; however,
the
mechanism for the increased PG formation during parturition has also not yet been explained and it is only conjectured that interleukin-1β(IL-1β), which shows a dramatic increase in the amnionic fluid of laboring women, stimulates the formation
of PG.
It is also suggested that infection may play an important role in preterm labor and that the signals from the fetus may initiate the labor. The purposes of this study are to find the effect of bacterial endotoxin and fetal urine on the synthesis
of
LI-1βby dispersed cells from human amnion and decidua, and to prove that IL-1βacts as an intermediate modulator of parturition. Amnions and deciduas were obtained from 5 cesarean-sectioned women before labor at term, and in each case
collagenase-dispersed amnion and decidual cells were incubated with bacterial endotoxin and fetal urine separately. There was a statistical difference in the level of IL-1βbetween the control and bacterial endotoxin-added groups with the
decidual
cell
cultures. On the other hand, the difference was not found in the amnion cell cultures. Fetal urine made no difference in the level of IL-1βwith the control group in both the amnion and decidual cell cultures.
By the results of this study, it is believed that IL-1βis produced by the decidual cells not by the amnion cells and that bacterial endotoxin in the amnionic fluid may induce the formation of IL-1β, the intermediate modulator of parturition.
The
results also show that fetal urine does'nt stimulate the formation of IL-1β
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