Amniotic fluid of primates contains a high concentration of prolactin (PRL) of decidual origin which decreases with intrauterine bacterial infection prior to preterm labor. Cytokines and prostaglandins (PGs) increase in amniotic fluid after infection in vivo and cytokines inhibit decidual PRL secretion in vitro. To determine whether cytokines or PGs mediate the effect of bacterial infection on PRL in the whole animal, chronically instrumented pregnant rhesus monkeys were prepared. Interleukin (IL)-1 (10 fg; 6 ml/h for 2 h) was infused into the amniotic cavity, alone (n=6) and during a longer term treatment with indomethacin (n=5). In animals which received both treatments serially (n=4), the infusion with indomethacin preceded the infusion of IL-1 alone because IL-1 can induce preterm labor. Amniotic fluid samples were obtained relative to infusion at -24 h and -1 h, then at least once during the following 24 h, and again between 25 h and 72 h. Samples were frozen at -20xC until assay for PRL. Amniotic fluid levels of IL-1 were verified and PGE2 and PGF2` were also measured. PRL levels were expressed as a percent of preinfusion values and compared by analysis of variance followed by pairwise comparison. IL-1 levels greater than 10 ng/ml were achieved due to infusion. PGs were unchanged during indomethacin treatment, but increased significantly following IL-1 alone. Prior to IL-1 infusion, PRL levels averaged 82 q 20 fg/ml. Infusion of IL-1 caused a 42% decrease in amniotic fluid PRL by 24 h (p<0.05 vs preinfusion) and a 66% decline by 72 h (p<0.05 vs 24 h). There was an increase in uterine activity at 6.0 q 2.4 h after infusion. Five of the 6 animals delivered at 74 q 29 h after infusion of IL-1 . Infusion of indomethacin for 48 h preceding IL-1 plus 60 h following IL-1 did not abolish the effect of IL-1 on the decline in PRL levels. PRL levels were 41% less than preinfusion values by 25-72 h post infusion (p<0.05) in the presence of indomethacin. Indomethacin did prevent the increase in uterine activity which was induced by IL-1 alone. In summary, IL-1 caused a decrease in amniotic fluid PRL in a manner similar to bacterial infection. Blockade of PG production prevented uterine contractions but it did not prevent the decline in amniotic fluid PRL. These results support the notion that IL-1 may act directly on decidual cells and inhibit PRL secretion.
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