AMNIOTIC-FLUID PROLACTIN IS DECREASED BY EXPERIMENTAL INTRAUTERINE INFECTION OR INTERLEUKIN-1-BETA INFUSION BUT NOT VIA PROSTAGLANDINS IN PREGNANT RHESUS MACAQUES

Amniotic fluid contains a high concentration of prolactin produced and secreted by the decidua. In vitro models have suggested that bacteria l products inhibit prolactin secretion by decidual cells. To further e xamine this potentially important regulatory mechanism in the whole an imal, chronically instrumented pregnant rhesus monkeys were prepared. Experimental infection was induced by intraamniotic or choriodecidual inoculation of 10(3)-10(6) group B streptococcus. Alternatively, inter leukin (IL)-1 beta was infused into the amniotic cavity. Finally, indo methacin was coadministered with IL-1 beta to block the production of prostaglandins (PGs), The average prolactin level prior to inoculation (0 h) equaled 34.0 +/- 6.4 mu g/ml. There was a 40% decrease in prola ctin by 37 h postinfection (n = 6) and a 71% decrease between 61 and 7 2 h postinfection (n = 3, p < 0.01 vs. before infection). Infusion of IL-1 beta also caused a decrease in amniotic fluid prolactin. There wa s a 42% decrease in prolactin between 0 and 24 h postinfusion (p < 0.0 5) and a 66% decrease between 25 and 72 h after IL-1 beta infusion (p < 0.05; n = 6). Coadministration of indomethacin with IL-1 beta preven ted the accompanying increase in PGs but did not prevent the decrease in prolactin (n = 5). Amniotic fluid prolactin levels in untreated mon keys were stable and without a prepartum decline during the sampling p eriod from 130 to 166 days of gestation. In summary, intrauterine bact erial infection decreases amniotic fluid prolactin, and IL-10 mimics t his effect. The effect of IL-1 beta on amniotic fluid prolactin does n ot appear to be mediated by PGs and may involve a direct effect of IL- 1 beta on decidual cells.