Bose, C., Laughon, M., Allred, E.N., Van Marter, L.J., O'shea, T.M., Ehrenkranz, R.A., Fichorova, R., Leviton, A; for the ELGAN Study Investigators.
Lung inflammation contributes to the pathogenesis of bronchopulmonary dysplasia (BPD) and may be accompanied by a systematic inflammatory response. The objective of this study was to investigate the role of systemic inflammation in the development of BPD in a cohort of extremely low GA newborns (ELGANs) by examining the relationships between inflammation-associated proteins in neonatal blood samples and pulmonary outcomes. Proteins were measured in blood specimens collected on postnatal d 1-3, 5-8, and 12-15 from 932 ELGANs. Increased risk of BPD was associated with elevated blood concentrations of a variety of proinflammatory cytokines, adhesion molecules, and proteases. Reduced risk was prominently associated with increased concentrations of one chemokine, RANTES. Elevations of inflammatory proteins associated with BPD risk occurred during the first days after birth and inflammation intensified thereafter. Therefore, exposures that promote inflammation after the first postnatal days may be more critical in the pathogenesis of BPD. Fetal growth restriction, a known BPD risk factor, was not accompanied by proteins elevations and therefore does not seem to be mediated by systemic inflammation. By contrast, mechanical ventilation altered protein levels and may be associated with systemic inﬂammation