We have previously described, in pregnant rhesus monkeys, the temporal relationships among amniotic fluid bacterial counts, cytokines, PGs, and increases in uterine contractility that have established a causal relationship between intraamniotic infection and premature labor in primates. This study provides new evidence that intrauterine bacterial infection with GBS decreases amniotic fluid levels of prolactin in a clear and progressive fashion. buy antibiotics online
The fall in prolactin was associated with an elevation in amniotic fluid PGE2 concentrations and with an increase in levels of the proinflammatory cytokines, IL-13 and TNFa. A similar decrease in amniotic fluid prolactin was observed when the cytokine IL-1(3 was infused into the amniotic cavity in the absence of infection. IL-1 (3 alone also elicited an increase in amniotic fluid PGE2 and often led to labor and delivery. While indomethacin blocked the IL-1 (3-induced rise in PGE2 and in uterine contractions, it did not prevent the decrease in amniotic fluid prolactin. These results provide the first in vivo evidence that intrauterine bacterial infection may increase proinflammatory cytokines that in turn directly inhibit prolactin production from the maternal decidua.