What is BPD in 2012 and what will BPD become?

The study aimed to evaluate the association between microbes in the lower respiratory tract (LRT) and the srisk for severe bronchopulmonary dysplasia (sBPD) in premature infants.

We conducted a retrospective, single-center study of preterm infants who were admitted to the neonatal intensive care unit (NICU) of Southern Medical University Affiliated Maternal & Child Health Hospital of Foshan, China, between January 2015 and December 2017. The microbes in the LRT were screened by using tracheobronchial aspirate fluid (TAF) culture.

One hundred and fifty-five infants were included in the analysis. Among 155 infants, 41 were diagnosed with sBPD, and 114 were diagnosed without sBPD. There were significant differences between infants with and without sBPD in regard to birth weight (BW), gestational age (GA), the duration of endotracheal ventilation and supplemental oxygen. The incidence of retinopathy (ROP) and sepsis was higher in the sBPD infants than in the infants without sBPD. There was a difference in the detection rate of Gram-negative bacteria (GNB) between the two groups. Stenotrophomonas maltophilia and Klebsiella pneumoniae were mainly detected in TAF.

The LRT microbes were different between infants with and without sBPD, and GNB is more frequently detected in sBPD infants.

Bronchopulmonary dysplasia (BPD) is a chronic lung disease with long-term sequelae including neurodevelopmental delay. Although the precise mechanism of BPD is not well defined, oxidative stress is thought to be involved in the pathogenesis process of BPD. Nrf2 (Nuclear factor erythroid 2-related factor 2)-Keap1 (Kelch-like ECH associated protein 1)-ARE (Antioxidant Reaction Elements) signaling pathway is one of the main protective mechanisms of BPD, which can induce cytoprotective gene expression, such as heme oxygenase‐1 (HO-1), nicotinamide quinone oxidoreductase 1 (NQO1) and so on. We exposed premature rats to hyperoxia and identified lung developmental retardation in preterm rats, with similar pathological changes as BPD. The expression of Nrf2 and HO-1 in premature rats was significantly higher after hyperoxia exposure. To explore the changes of Nrf2 and HO-1 in premature rats and enhance their beneficial functions may provide new treatment strategies for infants at risk of BPD.

Bronchopulmonary dysplasia (BPD) continues to be one of the most common complications of preterm birth and is characterized histopathologically by impaired lung alveolarization. Extremely preterm born infants remain at high risk for the development of BPD, highlighting a pressing need for continued efforts to understand the pathomechanisms at play in affected infants. This brief review summarizes recent progress in our understanding of the how the development of the newborn lung is stunted, highlighting recent reports on roles for growth factor signaling, oxidative stress, inflammation, the extracellular matrix and proteolysis, non-coding RNA, and fibroblast and epithelial cell plasticity. Additionally, some concerns about modeling BPD in experimental animals are reviewed, as are new developments in the in vitro modeling of pathophysiological processes relevant to impaired lung alveolarization in BPD.