Objectives: To investigate the association between serum N-terminal pro-B-type natriuretic peptide (NT-proBNP) level on the first day of life and a composite outcome of bronchopulmonary dysplasia (BPD) or death in a cohort of infants born before 32 weeks of gestation. Methods: We retrospectively identified infants born before 32 weeks of gestation who had serum NT-proBNP levels measured when they were admitted to the Neonatal Intensive Care Unit shortly after birth. The outcome of BPD or death was assessed at 36 weeks of postmenstrual age. The association of serum NT-proBNP levels with BPD or death was evaluated. Receiver operator characteristic (ROC) curve analysis was used to evaluate the predictive performance of serum NT-proBNP levels. Results: A 100 and 47 preterm infants had serum NT-proBNP levels measured on the first day of life. Serum NT-proBNP level was significantly higher in preterm infants who developed moderate/severe BPD or died [3,855 (2,567–6,369) vs. 1,259 (950–2,035) in control infants, P < 0.001]. On binary regression analysis, a high natural logarithm of serum NT-proBNP levels was associated with increased risk of moderate/severe BPD or death adjusted for gestational age, birth weight, birth weight z-score, and Apgar scores at 1 and 5 min (odds ratio [OR] = 5.195, 95% confidence interval [CI] 2.667–10.117, P < 0.001). ROC analysis identified a NT-proBNP level of 2002.5 pg/mL to have 87.5% sensitivity and 74.7% specificity for predicting moderate/severe BPD or death. The area under the curve (AUC) was 0.853 (95% CI 0.792–0.914). Conclusion: Serum NT-proBNP level measured on the first day of life is a promising biomarker for predicting the development of moderate/severe BPD or death in preterm infants. Our findings warrant a larger prospective study to incorporate measurement of NT-proBNP in prognosticating outcomes in very preterm infants.
Current treatments for inflammation associated with bronchopulmonary dysplasia (BPD) fail to show clinical efficacy. Foxm1, a transcription factor of the Forkhead box family, is a critical mediator of lung development and carcinogenesis, but its role in BPD-associated pulmonary inflammation is unknown. Immunohistochemistry and RNA analysis were used to assess Foxm1 in lung tissue from hyperoxia-treated mice and patients with BPD. LysM-Cre/Foxm1(-/-) mice, in which Foxm1 was deleted from myeloid-derived inflammatory cells, including macrophages, monocytes, and neutrophils, were exposed to neonatal hyperoxia, causing lung injury and remodeling. Measurements of lung function and flow cytometry were used to evaluate the effects of Foxm1 deletion on pulmonary inflammation and repair. Increased Foxm1 expression was observed in pulmonary macrophages of hyperoxia-exposed mice and in lung tissue from patients with BPD. After hyperoxia, deletion of Foxm1 from the myeloid cell lineage decreased numbers of interstitial macrophages (CD45(+)CD11b(+)Ly6C(-)Ly6G(-)F4/80(+)CD68(-)) and impaired alveologenesis and lung function. The exaggerated BPD-like phenotype observed in hyperoxia-exposed LysM-Cre/Foxm1(-/-) mice was associated with increased expression of neutrophil-derived myeloperoxidase, proteinase 3, and cathepsin g, all of which are critical for lung remodeling and inflammation. Our data demonstrate that Foxm1 influences pulmonary inflammatory responses to hyperoxia, inhibiting neutrophil-derived enzymes and enhancing monocytic responses that limit alveolar injury and remodeling in neonatal lungs.
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