Thus, the available data in women and in nonhuman primates suggest there is no pre-labor decline in amniotic fluid prolactin or in maternal, fetal, or amniotic fluid progesterone levels. Because decidual prolactin production is so closely regulated by progesterone, these data provide indirect evidence for the absence of a localized progesterone withdrawal mechanism at the level of the maternal decidua that would initiate parturition. Similarly, one could argue against an increase in endogenous cytokine production in the decidua and suggest that peripartum fluetuations in amniotic fluid prolactin are related to the consequences of labor and not the initiation of labor. This view is supported by our previous work in the rhesus monkey indicating that in the absence of infection, the spontaneous onset of labor is preceded by an increase in amniotic fluid PGE2 and PGF2„ but not in the concentrations of IL-13 or TNFa. Recent evidence also indicates that decidual tissue obtained from women in spontaneous labor at term exhibits a lower expression of interferon-7 and no increase in amniotic fluid type 1 (proinflammatory) cytokines. buy diabetes drugs
In conclusion, intraamniotic bacterial infection with GBS decreases amniotic fluid prolactin concentrations. Brief infusion of the proinflammatory cytokine, IL-1(3, into the amniotic cavity mimics the action of bacterial infection and causes a decrease in amniotic fluid prolactin. Blockade of PG synthesis with indomethacin did not prevent the IL-l|3-induced decrease in amniotic fluid prolactin.