According to the current view, the fetal membranes and the amniotic fluid are central in transmission of signals resulting in labor and delivery. It has also become increasingly evident that although preterm and term labor share common pathways in activation of uterine contractions, the regulatory aspects are fundamentally different. The present article is a brief overview focusing on the participation of prostaglandins in human term and preterm labor. The involvement of bacteria in preterm labor is presented. In addition, it is proposed that inflammatory polymorphonuclear leukocytes promote preterm labor by activating prostaglandin production from human fetal membranes.