Premature and, to a lesser extent, full term infants are at risk for development of infant respiratory distress syndrome (IRDS) due to deficient levels of pulmonary surfactant and to inactivation of surfactant by plasma proteins. Respiratory distress syndrome in neonatal patients is a devastating lung illness in newborns and young children, with high incidences of morbidity and mortality, and it is accompanied by tremendous emotional and financial expenses. In the U.S. alone, about 5000 infants die of IRDS every year. Acute lung injury in IRDS patients is characterized by lung inflammation, increased alveolar capillary membrane permeability, pulmonary edema, and progressive hypoxemia.

Thankfully, replacement therapies have been developed which supplement surfactant on the gas exchange surfaces of the lungs and mitigate some of the severe problems that are associated with IRDS. However, it is becoming clear that IRDS patients have additional, related problems due to increased lung levels of pro-inflammatory cytokines, and to the resultant lung inflammation. In the setting of IRDS, activated neutrophils exacerbate lung tissue injury and have been implicated in the development of bronchopulmonary dysplasia (BPD), which is a form of chronic lung disease that occurs in substantial numbers (20-30 percent) of premature infants recovering from IRDS. Notably, neonatal patients with elevated proinflammatory mediators and increased pulmonary inflammation are at increased risk to develop BPD, indicating that inflammation and neutrophil-derived products likely contribute to the pathogenesis of BPD. Recent experimental findings indicate that the mechanism of BPD development likely includes pulmonary inflammation and resultant lung damage from oxyradicals and enzymes from activated leukocytes. We hypothesize that transforming growth factor (TGF) may contribute to the lung problems associated with IRDS.

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