The enhanced production of placental interleukin-1 during labor and intrauterine infection.

The purpose of this study was to determine the effect of labor and chorioamnionitis in interleukin-1 production by human placenta. We studied the activity of the placenta to produce interleukin-1 with an enzyme immunoassay by culturing tissue blocks. The placental tissue obtained after labor produced a larger amount of interleukin-1 than placental tissue obtained before labor. All the placental tissues produced more interleukin-1 beta than interleukin-1 alpha. The placentas with labor and chorioamnionitis produced about seventeenfold more interleukin-1 than placentas with labor only. We immunohistochemically identified interleukin-1--producing cells in the placenta and found that syncytiotrophoblasts produced both interleukin-1 alpha and interleukin-1 beta, while Hofbauer cells produced only interleukin-1 beta. In vitro analysis of the trophoblast activities to produce interleukin-1 revealed that microbial byproducts enhanced interleukin-1 production, possibly inducing accumulation of interleukin-1 receptor-positive cells at the sites of inflammation. In addition to stimulation of prostaglandin biosynthesis and labor, the placental interleukin-1 may act as an inflammatory mediator, leading to systemic and local changes at fetomaternal interface and activating fetomaternal immune systems against intrauterine infection.