scholarly journals Caffeine and Bronchopulmonary dysplasia ：Clinical Benefits and Its Mechanisms

2021 ◽  
Author(s):  
Yuan Yuan ◽  
Yang yang ◽  
Xiaoping Lei ◽  
WENBIN DONG
Keyword(s):  
Bronchopulmonary Dysplasia ◽  
Lung Development ◽  
Chronic Respiratory Disease ◽  
Mechanisms Of Action ◽  
Clinical Value ◽  
Treatment Technology ◽  
Clinical Benefits ◽  
Apoptotic Pathways ◽  
Prevention Of Prematurity ◽  
Postnatal Factors

Bronchopulmonary dysplasia (BPD) is a chronic respiratory disease caused by a combination of prenatal and postnatal factors that leads to the disruption of lung development and abnormal repair, this is a condition that is commonly seen in premature infants. With the improvement of treatment technology, the survival rate of very early preterm infants has increased significantly compared with before, and the incidence of severe BPD has decreased, however, the prevalence of BPD has not decreased. The overall prevalence of BPD is 45%.The prevention of prematurity, the systematic use of non-aggressive ventilator measures, the avoidance of supra-physiological oxygen exposure, and the administration of diuretics, caffeine and vitamin A have all been shown to lead to a significant reduction in the risk of BPD development. A growing number of clinical studies have shown that caffeine not only prevents apnea, but also reduces the incidence of BPD. We review the clinical value of caffeine in the treatment of BPD and its potential mechanisms of action, include anti-inflammatory, antioxidant, anti-fibrotic, anti-apoptotic pathways, and the regulation of angiogenesis. Our aim was to provide a new theoretical basis for the clinical treatment of BPD.

scholarly journals Animal models of bronchopulmonary dysplasia. The term mouse models

2014 ◽  
Vol 307 (12) ◽  
pp. L936-L947 ◽  
Author(s):  
Jessica Berger ◽  
Vineet Bhandari
Keyword(s):  
Animal Models ◽  
Lung Injury ◽  
Mouse Models ◽  
Bronchopulmonary Dysplasia ◽  
Lung Development ◽  
Invasive Mechanical Ventilation ◽  
Therapeutic Interventions ◽  
Contributing Factors ◽  
Short Term ◽  
Injury Models

The etiology of bronchopulmonary dysplasia (BPD) is multifactorial, with genetics, ante- and postnatal sepsis, invasive mechanical ventilation, and exposure to hyperoxia being well described as contributing factors. Much of what is known about the pathogenesis of BPD is derived from animal models being exposed to the environmental factors noted above. This review will briefly cover the various mouse models of BPD, focusing mainly on the hyperoxia-induced lung injury models. We will also include hypoxia, hypoxia/hyperoxia, inflammation-induced, and transgenic models in room air. Attention to the stage of lung development at the timing of the initiation of the environmental insult and the duration of lung injury is critical to attempt to mimic the human disease pulmonary phenotype, both in the short term and in outcomes extending into childhood, adolescence, and adulthood. The various indexes of alveolar and vascular development as well as pulmonary function including pulmonary hypertension will be highlighted. The advantages (and limitations) of using such approaches will be discussed in the context of understanding the pathogenesis of and targeting therapeutic interventions to ameliorate human BPD.

Mechanisms of Lung Injury and Bronchopulmonary Dysplasia

2016 ◽  
Vol 33 (11) ◽  
pp. 1076-1078 ◽  
Author(s):  
Alan Jobe
Keyword(s):  
Birth Weight ◽  
Lung Injury ◽  
Bronchopulmonary Dysplasia ◽  
Gestational Age ◽  
Lung Development ◽  
Complex Disease ◽  
Extremely Low Birth Weight ◽  
Tobacco Exposure ◽  
Good Definition ◽  
Injury And Repair

Although bronchopulmonary dysplasia (BPD) is the most frequent adverse outcome for infants born at < 30 weeks gestational age, there remain major gaps in understanding the pathophysiology, and thus there are few effective targeted therapies to prevent and treat BPD. This review will focus on the substantial problems and knowledge gaps for the clinician and investigator when considering lung injury and BPD. The epidemiology of BPD is clear: BPD is a lung injury syndrome predominantly in extremely low-birth-weight infants with an incidence that increases as gestation/birth weight decrease, with growth restriction, in males and with fetal exposures and with injury from postdelivery respiratory care. However, we do not have a good definition of BPD that identifies the infants that die of respiratory disease before 36 weeks or that predicts long-term outcomes as well. The injury resulting in BPD likely begins as altered lung development before delivery in many infants (small for gestational age, chorioamnionitis, tobacco exposure), can be initiated by resuscitating at birth, and then amplified by postnatal exposures (oxygen, mechanical ventilation, infection). Conceptually the events leading to BPD are the continued interplay of lung development that is altered progressively by injury and repair to result in poorly defined phenotypes of BPD. The injury pathways prominently cause inflammation, and as a proof of principle, corticosteroids can decrease the incidence and severity of BPD, as demonstrated by three recent trials of the early use of steroids. There are likely “adaptation” and “tolerance” responses that modulate the injury and repair to increase or decrease the damage, interactions that are not understood. BPD is a more complex disease.

Altered lung development in bronchopulmonary dysplasia

2014 ◽  
Vol 100 (3) ◽  
pp. 158-167 ◽  
Author(s):  
Alice Hadchouel ◽  
Marie-Laure Franco-Montoya ◽  
Christophe Delacourt
Keyword(s):  
Bronchopulmonary Dysplasia ◽  
Lung Development

scholarly journals Deregulation of the lysyl hydroxylase matrix cross-linking system in experimental and clinical bronchopulmonary dysplasia

2014 ◽  
Vol 306 (3) ◽  
pp. L246-L259 ◽  
Author(s):  
Thilo J. Witsch ◽  
Paweł Turowski ◽  
Elpidoforos Sakkas ◽  
Gero Niess ◽  
Simone Becker ◽  
...  
Keyword(s):  
Animal Model ◽  
Bronchopulmonary Dysplasia ◽  
Experimental Animal ◽  
Lung Development ◽  
Lung Epithelial Cells ◽  
Experimental Animal Model ◽  
Lung Fibroblasts ◽  
Normal Lung ◽  
Mrna Levels ◽  
Lysyl Hydroxylase

Bronchopulmonary dysplasia (BPD) is a common and serious complication of premature birth, characterized by a pronounced arrest of alveolar development. The underlying pathophysiological mechanisms are poorly understood although perturbations to the maturation and remodeling of the extracellular matrix (ECM) are emerging as candidate disease pathomechanisms. In this study, the expression and regulation of three members of the lysyl hydroxylase family of ECM remodeling enzymes (Plod1, Plod2, and Plod3) in clinical BPD, as well as in an experimental animal model of BPD, were addressed. All three enzymes were localized to the septal walls in developing mouse lungs, with Plod1 also expressed in the vessel walls of the developing lung and Plod3 expressed uniquely at the base of developing septa. The expression of plod1, plod2, and plod3 was upregulated in the lungs of mouse pups exposed to 85% O2, an experimental animal model of BPD. Transforming growth factor (TGF)-β increased plod2 mRNA levels and activated the plod2 promoter in vitro in lung epithelial cells and in lung fibroblasts. Using in vivo neutralization of TGF-β signaling in the experimental animal model of BPD, TGF-β was identified as the regulator of aberrant plod2 expression. PLOD2 mRNA expression was also elevated in human neonates who died with BPD or at risk for BPD, compared with neonates matched for gestational age at birth or chronological age at death. These data point to potential roles for lysyl hydroxylases in normal lung development, as well as in perturbed late lung development associated with BPD.

The impact of vitamin D on fetal and neonatal lung maturation. A systematic review

2015 ◽  
Vol 308 (7) ◽  
pp. L587-L602 ◽  
Author(s):  
Sine Lykkedegn ◽  
Grith Lykke Sorensen ◽  
Signe Sparre Beck-Nielsen ◽  
Henrik Thybo Christesen
Keyword(s):  
Vitamin D ◽  
Respiratory Distress Syndrome ◽  
Respiratory Distress ◽  
Bronchopulmonary Dysplasia ◽  
Lung Development ◽  
Distress Syndrome ◽  
Hypovitaminosis D ◽  
Laboratory Studies ◽  
Lung Maturation ◽  
The Impact

Respiratory distress syndrome (RDS) and bronchopulmonary dysplasia (BPD) are major complications to preterm birth. Hypovitaminosis D is prevalent in pregnancy. We systematically reviewed the evidence of the impact of vitamin D on lung development, surfactant synthesis, RDS, and BPD searching PubMed, Embase, and Cochrane databases with the terms vitamin D AND (surfactant OR lung maturation OR lung development OR respiratory distress syndrome OR fetal lung OR prematurity OR bronchopulmonary dysplasia). Three human studies, ten animal studies, two laboratory studies, and one combined animal and laboratory study were included. Human evidence was sparse, allowing no conclusions. BPD was not associated with vitamin D receptor polymorphism in a fully adjusted analysis. Animal and laboratory studies showed substantial positive effects of vitamin D on the alveolar type II cell, fibroblast proliferation, surfactant synthesis, and alveolarization. These data support the hypothesis of hypovitaminosis D as a frequent, modifiable risk factor of RDS and BPD, which should be tested in randomized controlled trials on pregnant women, those with threatening preterm delivery, or in the preterm neonates. Future experimental and human studies should aim to identify optimal time windows, vitamin D doses, and cut-off levels for 25-hydroxyvitamin D in interventions against RDS, BPD, and later adverse respiratory outcomes.

Recent advances in late lung development and the pathogenesis of bronchopulmonary dysplasia

2013 ◽  
Vol 305 (12) ◽  
pp. L893-L905 ◽  
Author(s):  
Alicia Madurga ◽  
Ivana Mižíková ◽  
Jordi Ruiz-Camp ◽  
Rory E. Morty
Keyword(s):  
Gas Exchange ◽  
Surface Area ◽  
Bronchopulmonary Dysplasia ◽  
Lung Development ◽  
Oxygen Toxicity ◽  
Structural Development ◽  
Vascular Structure ◽  
Recent Developments ◽  
Immature Lung ◽  
Prematurely Born Infants

In contrast to early lung development, a process exemplified by the branching of the developing airways, the later development of the immature lung remains very poorly understood. A key event in late lung development is secondary septation, in which secondary septa arise from primary septa, creating a greater number of alveoli of a smaller size, which dramatically expands the surface area over which gas exchange can take place. Secondary septation, together with architectural changes to the vascular structure of the lung that minimize the distance between the inspired air and the blood, are the objectives of late lung development. The process of late lung development is disturbed in bronchopulmonary dysplasia (BPD), a disease of prematurely born infants in which the structural development of the alveoli is blunted as a consequence of inflammation, volutrauma, and oxygen toxicity. This review aims to highlight notable recent developments in our understanding of late lung development and the pathogenesis of BPD.

Risk Factors for the Degradation of Lung Elastic Fibers in the Ventilated Neonate: Implications for Impaired Lung Development in Bronchopulmonary Dysplasia

1992 ◽  
Vol 146 (1) ◽  
pp. 204-212 ◽  
Author(s):  
Margaret C. Bruce ◽  
Mark Schuyler ◽  
Richard J. Martin ◽  
Barry C. Starcher ◽  
Joseph F. Tomashefski ◽  
...  
Keyword(s):  
Risk Factors ◽  
Bronchopulmonary Dysplasia ◽  
Lung Development ◽  
Elastic Fibers

scholarly journals Clinical Utility of Whole Exome Sequencing and Targeted Panels for the Identification of Inborn Errors of Immunity in a Resource-Constrained Setting

2021 ◽  
Vol 12 ◽  
Author(s):  
Clair Engelbrecht ◽  
Michael Urban ◽  
Mardelle Schoeman ◽  
Brandon Paarwater ◽  
Ansia van Coller ◽  
...  
Keyword(s):  
Genetic Counselling ◽  
Molecular Diagnosis ◽  
Single Gene ◽  
Clinical Value ◽  
Inborn Errors ◽  
Detection Rates ◽  
Inborn Errors Of Immunity ◽  
Clinical Benefits ◽  
Gene Panels ◽  
Next Generation Sequencing Ngs

Primary immunodeficiency disorders (PIDs) are inborn errors of immunity (IEI) that cause immune system impairment. To date, more than 400 single-gene IEI have been well defined. The advent of next generation sequencing (NGS) technologies has improved clinical diagnosis and allowed for discovery of novel genes and variants associated with IEI. Molecular diagnosis provides clear clinical benefits for patients by altering management, enabling access to certain treatments and facilitates genetic counselling. Here we report on an 8-year experience using two different NGS technologies, namely research-based WES and targeted gene panels, in patients with suspected IEI in the South African healthcare system. A total of 52 patients’ had WES only, 26 had a targeted gene panel only, and 2 had both panel and WES. Overall, a molecular diagnosis was achieved in 30% (24/80) of patients. Clinical management was significantly altered in 67% of patients following molecular results. All 24 families with a molecular diagnosis received more accurate genetic counselling and family cascade testing. Results highlight the clinical value of expanded genetic testing in IEI and its relevance to understanding the genetic and clinical spectrum of the IEI-related disorders in Africa. Detection rates under 40% illustrate the complexity and heterogeneity of these disorders, especially in an African population, thus highlighting the need for expanded genomic testing and research to further elucidate this.

Sign in / Sign up

Export Citation Format

Share Document