Inflammatory pathways between placenta and foetus.

Recent evidence indicates that intra-amniotic endotoxin (LPS) and interleukin-1 alpha (IL-1alpha) accelerate foetal lung maturity and protect from respiratory distress syndrome (RDS) more effectively than does antenatal glucocorticoid. Inflammatory cytokines promote development of chronic lung disease in the premature, acute RDS (ARDS) in children and adults. Systemic exposure to LPS or cytokines can result in generalized multiorgan damage. The abnormal host defence in the foetus and the premature newborn need to be considered in therapeutic interventions.