Chorioamnionitis and inflammatory disease in the premature newborn infant

Preterm births occurs in 6-12% of all pregnancies, accounts for 75% of neonatal death and causes significant neonatal morbidity. A large number of preterm birth is associated with infection (30%), because of the release of many cytokines. In fact acute chorioamnionitis represents the inflammatory response to extracellular microorganisms that gain access to the gestational sac. Clinical signs of infection compare in the 12% of cases, while the prevalence of positive amniotic fluid cultures is approximately 50% in patients with preterm PROM. Despite the recent studies about the dosage of inflammatory biomarkers in the amniotic fluid or in fetal and maternal blood, placenta histology remains the gold standard for the diagnosis of chorioamnionitis. Histological chorioamnionitis describes the progression of the inflammatory process. Organisms first colonise the chorioamnionic surface. Then, the neutrophils migrates to the chorion (chorionitis) and to the amnion (chorioamnionitis) and, in the last stage, amnionic epithelial cells undergo necrosis (necrotising chorioamnionitis). It represents the mother inflammatory response and it differs from the fetal inflammatory response (funisitis). Funisitis first appears in vessels of the chorionic plate (chorionic vasculitis) or in the umbilical vein (umbilical phlebitis), then in the umbilical artery (umbilical arteritis), and in the Wharton's jelly (umbilical perivasculitis). The fetal inflammatory response has been associated with inflammatory diseases of preterm infants, increasing the risk of neonatal sepsis and meningitis, bronchopulmonary dysplasia and cerebral palsy. We present our experience on the relationship between histological chorioamnionitis, preterm birth and inflammatory diseases of VLBW infants.