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 bacterial products inhibit prolactin secretion by decidual cells. To further examine this potentially important regulatory mechanism in the whole animal, 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, interleukin (IL)-1(beta) was infused into the amniotic cavity. Finally, indomethacin 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 microg/ml. There was a 40% decrease in prolactin by 37 h postinfection (n = 6) and a 71% decrease between 61 and 72 h postinfection (n = 3, p < 0.01 vs. before infection). Infusion of IL-1(beta) also caused a decrease in amniotic fluid prolactin. There was a 42% decrease in prolactin between 0 and 24 h postinfusion (p < 0.05) 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) prevented the accompanying increase in PGs but did not prevent the decrease in prolactin (n = 5). Amniotic fluid prolactin levels in untreated monkeys were stable and without a prepartum decline during the sampling period from 130 to 166 days of gestation. In summary, intrauterine bacterial infection decreases amniotic fluid prolactin, and IL-1(beta) mimics this effect. The effect of IL-1(beta) on amniotic fluid prolactin does not appear to be mediated by PGs and may involve a direct effect of IL-1(beta) on decidual cells