Bronchopulmonary Dysplasia

Kair, Laura R.; Leonard, Douglas; Anderson, JoDee M.; MEd,

doi:10.1542/pir.33-6-255

Cited by 48 publications

(45 citation statements)

References 32 publications

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“…Characterized by multifactorial chronic lung disease, it may affect not only pulmonary function, but also growth, cardiovascular health and neurodevelopment (1). Although the mechanism of BPD yet remains to be clarified, chorioamnionitis, sepsis, invasive mechanical ventilation and hyperoxia may contribute to its incidence (2).…”

Section: Introductionmentioning

confidence: 99%

Vitamin D attenuates hyperoxia-induced lung injury through downregulation of Toll-like receptor 4

Yao

Shi

Zhao

et al. 2017

International Journal of Molecular Medicine

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With considerable morbidity and mortality, bron-chopulmonary dysplasia (BPD) is a focus of attention in neonatology. Hyperoxia-induced lung injury has long been used as a model of BPD. Among all the signaling pathways involved, Toll-like receptor 4 (TLR4) has been demonstrated to play an important role, and is known to be regulated by vitamin D. This study aimed at elucidating the effect of vitamin D on hyperoxia-induced lung injury and the role of TLR4 in the process. Vitamin D was administered to hyperoxia-treated neonatal rats to investigate changes in the morphology of lungs and expression of pro-inflammatory cytokines, apoptotic proteins and TLR4. Vitamin D attenuated hyperoxia-induced lung injury by protecting the integrity of the lung structure, decreasing extracellular matrix deposition and inhibiting inflammation. The upregulation of TLR4 by hyperoxia was ameliorated by vitamin D and apoptosis was reduced. Vitamin D administration antagonized the activation of TLR4 and therefore alleviated inflammation, reduced apoptosis and preserved lung structure.

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Section: Introductionmentioning

confidence: 99%

Vitamin D attenuates hyperoxia-induced lung injury through downregulation of Toll-like receptor 4

Yao

Shi

Zhao

et al. 2017

International Journal of Molecular Medicine

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“…The overall aim of the clinical research is to identify novel preventive and therapeutic strategies for BPD. It has been documented that vitamin A supplementation in extremely low birth weight infants and caffeine therapy for apnea of prematurity are effective in reducing the incidence of BPD [39]. Our findings will contribute to identifying preterm infants at high risk of BPD who could benefit the most from the prophylactic administration of vitamin A and caffeine during the early period of life.…”

Section: Discussionmentioning

confidence: 60%

“…Surfactant therapy is a standard of care for infants at risk of RDS. Although current evidence is insufficient to support surfactant treatment strategies for the prevention of BPD [4,39], the surfactant with brief ventilation as part of the intubation surfactant extubation approach was found to reduce the rates of BPD [40]. Surfactant use included in the model is likely not causal for BPD or death but reflective of respiratory illness or management.…”

Section: Discussionmentioning

confidence: 99%

Addition of SNAP to perinatal risk factors improves the prediction of bronchopulmonary dysplasia or death in critically ill preterm infants

Yan

et al. 2013

BMC Pediatr

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BackgroundBronchopulmonary dysplasia (BPD) is the most common serious pulmonary morbidity in premature infants. The score for neonatal acute physiology (SNAP) is a physiologic severity index for neonatal intensive care and correlates well with neonatal mortality and clinical outcomes. The prognostic value of the SNAP score for BPD in preterm infants remains to be clarified. The aim of the study was to determine whether SNAP can predict the development of BPD or death, and to investigate the contribution of SNAP to the predictive accuracy of other potential perinatal risk factors for the adverse outcome in critically ill preterm infants.MethodsWe conducted a study in 160 critically ill preterm infants with less than 33 gestational weeks. The original SNAP score was prospectively calculated based on 28 items collected during the first 24 hours of admission. The potential perinatal risk factors were assessed during the first 72 hours of life. Major outcome measures were BPD and mortality before the time of BPD screening.ResultsOf the 160 infants, 17 died and 41 developed BPD. The SNAP score was significantly associated with BPD or death (odds ratio [OR] =1.28; 95% confidence interval [CI], 1.16-1.41; p <0.001), even after adjustment for gestational age (OR =1.27; 95% CI, 1.13-1.41; p <0.001). High SNAP score was an independent predictor of BPD or death (area under the curve [AUC] =0.78; 95% CI, 0.70-0.85; p <0.001), with additional predictive value when combined with other perinatal risk factors. Multivariate regression analysis resulted in a final model, including SNAP, gestational age, apnea of prematurity, patent ductus arteriosus, and surfactant use as independent risk factors, with a higher predictive accuracy compared with individual components (AUC =0.92; 95% CI, 0.87-0.96; p <0.001).ConclusionsSNAP is associated with adverse outcome of BPD or death. High SNAP scores are predictive of BPD or death in critically ill preterm infants, and add prognostic value to other perinatal risk factors.

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“…While the severity of RDS in preterm born infants has decreased in recent decades with better pre-and postnatal care including the application of antenatal corticosteroids, postnatal surfactant supplementation, and more gentle modes of mechanical ventilations (Jobe 1993), the incidence of BPD has only minimally changed (Kair 2012). Despite the growing knowledge of inflammatory (Bose 2008) and oxidative injury (Saugstad 2003) contributing to BPD pathogenesis, treatment options for BPD still have limited success (Beam 2014).…”

Section: Introductionmentioning

confidence: 99%

Interdependent TTF1 - ErbB4 interactions are critical for surfactant protein-B homeostasis in primary mouse lung alveolar type II cells

Marten

Nielsen

Dammann

2015

J. Cell Commun. Signal.

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ErbB4 receptor and thyroid transcription factor (TTF)-1 are important modulators of fetal alveolar type II (ATII) cell development and injury. ErbB4 is an upstream regulator of TTF-1, promoting its expression in MLE-12 cells, an ATII cell line. Both proteins are known to promote surfactant protein-B gene (SftpB) and protein (SP-B) expression, but their feedback interactions on each other are not known. We hypothesized that TTF-1 expression has a feedback effect on ErbB4 expression in an in-vitro model of isolated mouse ATII cells. We tested this hypothesis by analyzing the effects of overexpressing HER4 and Nkx2.1, the genes of ErbB4 and TTF-1 on TTF-1 and ErbB4 protein expression, respectively, as well as SP-B protein expression in primary fetal mouse lung ATII cells. Transient ErbB4 protein overexpression upregulated TTF-1 protein expression in primary fetal ATII cells, similarly to results previously shown in MLE-12 cells. Transient TTF-1 protein overexpression down regulated ErbB4 protein expression in both cell types. TTF-1 protein was upregulated in primary transgenic ErbB4-depleted adult ATII cells, however SP-B protein expression in these adult transgenic ATII cells was not affected by the absence of ErbB4. The observation that TTF-1 is upregulated in fetal ATII cells by ErbB4 overexpression and also in ErbB4-deleted adult ATII cells suggests additional factors interact with ErbB4 to regulate TTF-1 levels. We conclude that the interdependency of TTF-1 and ErbB4 is important for surfactant protein levels. The interactive regulation of ErbB4 and TTF-1 needs further elucidation.

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Bronchopulmonary Dysplasia

Cited by 48 publications

References 32 publications

Vitamin D attenuates hyperoxia-induced lung injury through downregulation of Toll-like receptor 4

Vitamin D attenuates hyperoxia-induced lung injury through downregulation of Toll-like receptor 4

Addition of SNAP to perinatal risk factors improves the prediction of bronchopulmonary dysplasia or death in critically ill preterm infants

Interdependent TTF1 - ErbB4 interactions are critical for surfactant protein-B homeostasis in primary mouse lung alveolar type II cells

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