Maternal-fetal interactions involve various hematological and immunological abnormalities, some of which have only recently been clarified. Although maternal infections and chorioamnionitis are known for some time, the recent demonstration of the role of placental infections in maternal and fetal cytokine production and on activation of labor sheds new light on the origin of certain diseases of the newborn infant. Indeed, chorioamnionitis is followed by elevated proinflammatory cytokine levels in the mother and newborn and may be responsible for premature delivery and neonatal asphyxia. Investigations into feto-maternal interactions related to cytokine release have demonstrated that interleukins are intimately connected with the onset of labor and the activation of superoxide anion release by professional phagocytes. Increased inflammatory mediators in the fetus and newborn can cause tissue damage and lung inflammatory injury, and play a key role in the development of RDS and chronic lung disease. In our experience, increased IL-1 beta, IL-6 and IFN-gamma can be found in the mother during labor and increased IL-6 in the newborn during the first hours of life. This increase has been associated with increased superoxide release by WBC of mothers and newborns. Our studies on the the relations between subclinical chorioamnionitis and neonatal outcome have revealed histological chorioamnionitis in 62% of all premature deliveries, and 50% of RDS cases. In particular, in preterm infants, histological chorioamnionitis has been associated with fetal tachycardia, metabolic acidosis, and immune acute phase response at birth. Histological chorioamnionitis may also be responsible for a sharp increase in fetal erythropoietin production leading for an increase in nucleated red blood cells(NRBC) in the fetus and newborn. In 251 newborns with gestational ages of 24-41 weeks, we found a significant correlation between the number of NRBC and the other markers of intrauterine asphyxia and brain damage. In conclusion, maternal infections and placental abnormalities may be followed by abnormally elevated inflammatory mediators and increased erythropoiesis.