Bronchopulmonary dysplasia (BPD) is a chronic inflammatory lung disease of very-lowbirth-weight (VLBW) preterm infants, associated with arrested lung development and a need for supplemental oxygen. Over the past few decades, the incidence of BPD has significantly raised as a result of improved survival of VLBW infants requiring mechanical ventilation. While early disease detection is critical to prevent chronic lung remodeling and complications later in life, BPD is often difficult to diagnose and prevent due to the lack of good biomarkers for identification of infants at risk, and overlapping symptoms with other diseases, such as pulmonary hypertension (PH). Due to the current lack of effective treatment available for BPD and PH, research is currently focused on primary prevention strategies, and identification of biomarkers for early diagnosis, that could also represent potential therapeutic targets. In addition, novel histopathological, biochemical, and molecular factors have been identified in the lung tissue and in biological fluids of BPD and PH patients that could associate with the disease phenotype. In this review, we provide an overview of biomarkers for pediatric BPD and PH that have been identified in clinical studies using various biological fluids. We also present a brief summary of the information available on current strategies and guidelines to prevent and diagnose BPD and PH, as well as their pathophysiology, risk factors, and experimental therapies currently available.

ronchopulmonary dysplasia (BPD) is the most common morbidity of preterm birth affecting 50% of infants born less than 30 weeks' gestation in the US. 1 Despite preventive efforts, the incidence of BPD is increasing owing to the improved survival of infants born extremely preterm. 2 Recent studies suggest racial disparities may adversely affect outcomes for preterm infants experiencing common neonatal morbidities, including respiratory distress syndrome, intraventricular hemorrhage, and necrotizing enterocolitis, during the initial neonatal intensive care unit (NICU) hospitalization. [3][4][5] However, our knowledge of the association of racial disparities with outcomes for preterm infants with BPD remains unclear.Multiple prospective cohort studies have determined that Black maternal race is independently associated with a de-creased risk of severe BPD at 36 weeks' postmenstrual age (PMA), when the diagnosis of BPD is made. 6,7 Additional analyses of these cohorts, however, also identify Black maternal race as an independent risk factor for increased respiratory morbidity in early childhood. 6,8,9 The mechanisms underlying the finding that preterm infants born to Black mothers are at decreased risk of developing severe BPD but are nonetheless at increased risk of early childhood respiratory morbidity remain unknown.The 2001 National Institutes of Health (NIH) consensus criteria define severe BPD in infants born less than 32 weeks' gestation as the need for supplemental oxygen for 28 days or more and a fraction of inspired oxygen greater than 0.3 and/or positive pressure at 36 weeks' PMA. 10 Short-and long-term outcomes for patients with BPD are highly variable. In this study, IMPORTANCE Bronchopulmonary dysplasia (BPD) is the most common serious morbidity of preterm birth. Short-term respiratory outcomes for infants with the most severe forms of BPD are highly variable. The mechanisms that explain this variability remain unknown and may be mediated by racial disparities.OBJECTIVE To determine the association of maternal race with death and length of hospital stay in a multicenter cohort of infants with severe BPD.

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Background: Cystic Fibrosis (CF) is the most common life limiting genetic disorder, characterized by chronic respiratory failure secondary to inflammation and chronic bacterial lung infection. Pseudomonas aeruginosa lung infection is associated with more severe lung disease and rapid progression of respiratory failure when compared to Staphylococcus aureus infection. We hypothesized that a specific signature of epigenetic factors targeting specific gene transcripts contributes to the increased morbidity seen in CF patients with chronic Pseudomonas infection. Methods: We collected exhaled breath condensate (EBC) from 27 subjects and evaluated miRNA signatures in these samples using commercial PCR array. We identified predicted mRNA targets and associated signaling pathways using Ingenuity Pathway Analysis. Results: We found 11 differentially expressed miRNAs in EBC of patients infected with Pseudomonas aeruginosa compared to EBC from CF patients who were not chronically infected with Pseudomonas aeruginosa (p < 0.05). Six of these miRNAs (hsa-miRNA-1247, hsa-miRNA-1276, hsa-miRNA-449c, hsa-miRNA-3170, hsa-miRNA-432-5p and hsa-miR-548) were significantly different in the CF Pseudomonas positive group when compared to both the CF Pseudomonas negative group and healthy control group. Ingenuity pathway analysis (IPA) revealed organismal injury and abnormalities, reproductive system disease and cancer as the top diseases and bio functions associated with these miRNAs. IPA also detected RELA,