**Abstract**

Half of all preterm births are caused or triggered by an inflammation at fetal-maternal interface. The sustained inflammation that preterm neonates are exposed is generated by maternal chorioamnionitis, premature rupture of membranes. This inflammation will facilitate the preterm labor, but also plays an important role in development of disease like: bronchopulmonary dysplasia, necrotizing enterocolitis, retinopathy of prematurity, intraventricular hemorrhage and periventricular leukomalacia. Preterm neonates have immature immune system. The fragile coregulation between immune defense mechanisms and immunosuppression (tolerance) is often disturbed at this category of patients. They are at high risk of sepsis due to this imbalance between the defense and suppression mechanisms but also several injuries can contribute to the onset or perpetuation of sustained inflammation. They experience altered antigen exposure in contact with hospital-specific germs, artificial devices, drugs, nutritional antigens, and hypoxia or hyperoxia. This is more significant at extremely preterm infants less than 28 weeks of gestation as they have not developed adaptation processes to tolerate maternal and self-antigens.

**Keywords:** preterm birth, inflammation, chorioamnionitis, premature rupture of membranes
