Neonatal respiratory morbidity continues to be an important cause of early-life morbidity, and is traditionally explained by the developing lung's structural and mechanical immaturity. However, the more evidence grows about the role of immune dysregulation during the perinatal period and its critical importance to respiratory adaptation, the more this explanation may need to change. In this study, we focus on the correlation of the severity of respiratory morbidity to inflammatory cytokine levels in neonatal and cord blood. Using multiplex cytokine analysis along with hierarchical clustering, several levels of modeling, and predictive analysis, we were able to characterize distinct inflammatory signatures in morbid neonates and compared them to the absence of morbid conditions at all levels. The association of higher levels of pro-inflammatory cytokines and lower levels of counter-regulatory ones to the need for more oxygen and the lung machine, further respiratory distress, the incidence of bronchopulmonary dysplasia, and the need for longer ventilation is described. The burden of composite inflammation showed to provide more accurate models for a morbid condition's prediction than linear models for the respiratory outcomes. The evidence allows for a prediction of the inflammatory signatures to serve as an important early assessment of the at risk condition pre- and post- birth.