Acute lung injury (ALI) results in high morbidity and mortality among
preterm neonates and efforts have therefore been devoted to both
antenatal and postnatal prevention of the disease. ALI is the result of
an inflammatory response which is triggered by a variety of different
mechanisms. It mostly affects the fetal lung and, in particular, causes
damage to the integrity of the lung’s alveolar-capillary unit while
weakening its cellular linings. Chemotactic activity and inflammatory
products, such as proinflammatory cytokines TNF-alpha, IL-1, IL-6,
IL-11, VEGF, TGF-alpha and TGF-beta, provoke serious damage to the
capillary endothelium and the alveolar epithelium, resulting in hyaline
membrane formation and leakage of protein-rich edema fluid into the
alveoli. Chorioamnionitis plays a major part in triggering fetal lung
inflammation, while mechanical ventilation, the application of which is
frequently necessary in preterm neonates, also causes ALI by inducing
proinflammatory cytokines. Many different ventilation-strategies have
been developed in order to reduce potential lung injury. Furthermore,
tissue injury may occur as a result of injurious oxygen by-products
(Reactive Oxygen Species, ROS), secondary to hyperoxia. Knowledge of the
inflammatory pathways that connect intra-amniotic inflammation and ALI
can lead to the formulation of novel interventional procedures. Future
research should concentrate on the pathophysiology of ALI in preterm
neonates and on possible pharmaceutical interventions targeting
prevention and/or resolution of ALI
