Evidence of unexpected oxidative stress in airways of adolescents born very pre-term

Filippone, Marco; Bonetto, G.; Corradi, Massimo; Frigo, Anna Chiara; Baraldi, Eugenio

doi:10.1183/09031936.00185511

Cited by 105 publications

(91 citation statements)

References 42 publications

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“…Such data support the hypothesis that airflow limitation in BPD survivors is unrelated to any asthma-like inflammation [16,19], indicating that another pathogenetic mechanism must be involved [19,20]. Recent reports have also suggested that prematurity may be associated with neutrophilic airway inflammation and oxidative stress later in life [21,22,23]. Available data thus support the hypothesis that the pathophysiological mechanisms behind airflow limitation in BPD and asthma probably stem from distinct mechanisms which need to be further investigated [24].…”

Section: Clinical Aspects and Functional Course Of Bpd With Agesupporting

confidence: 71%

Chronic Lung Disease of Prematurity: Long-Term Respiratory Outcome

et al. 2014

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Chronic respiratory morbidity is a common adverse outcome of preterm birth, especially in infants who develop bronchopulmonary dysplasia (BPD), which is still a major cause of long-term lung dysfunction with a heavy burden on health care services and medical resources throughout childhood. The most severely affected patients remain symptomatic even in adulthood, and this may be influenced also by environmental variables (e.g. smoking), which can contribute to persistent obstruction of airflow. Of all obstructive lung diseases in humans, BPD has the earliest onset and probably lasts the longest. Since the prevention of BPD is an elusive goal, minimizing neonatal lung injury and closely monitoring survivors remain the best courses of action. This review describes the clinical and functional changes characteristic of the long-term pulmonary sequelae of preterm birth, focusing particularly on BPD.

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Section: Clinical Aspects and Functional Course Of Bpd With Agesupporting

confidence: 71%

Chronic Lung Disease of Prematurity: Long-Term Respiratory Outcome

et al. 2014

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“…hyperoxia; lung development; premature birth BRONCHOPULMONARY DYSPLASIA (BPD) is the most common chronic lung disease of very preterm infants. BPD interrupts lung development and has serious long-term respiratory complications that reach beyond childhood and into adult life (8,25,26,41,53). The multifactorial etiology of BPD has prompted research to investigate the many factors contributing to the pathogenesis of BPD (reviewed in Ref.…”

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confidence: 99%

“…Recent evidence shows that BPD has long-term respiratory complications, which reach beyond childhood and into adult life, with follow-up studies demonstrating increased risk of respiratory symptoms (i.e., cough, wheeze), poor lung function, and low exercise capacity (8,18,25,26,41,53,69). Therefore, longterm studies in experimental models are now gaining greater interest.…”

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Animal models of bronchopulmonary dysplasia. The term rat models

O’Reilly

Thébaud

2014

American Journal of Physiology-Lung Cellular and Molecular Phys

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O'Reilly M, Thébaud B. Animal models of bronchopulmonary dysplasia. The term rat models. Am J Physiol Lung Cell Mol Physiol 307: L948 -L958, 2014. First published October 10, 2014; doi:10.1152/ajplung.00160.2014.-Bronchopulmonary dysplasia (BPD) is the chronic lung disease of prematurity that affects very preterm infants. Although advances in perinatal care have enabled the survival of infants born as early as 23-24 wk of gestation, the challenge of promoting lung growth while protecting the ever more immature lung from injury is now bigger. Consequently, BPD remains one of the most common complications of extreme prematurity and still lacks specific treatments. Progress in our understanding of BPD and the potential of developing therapeutic strategies have arisen from large (baboons, sheep, and pigs) and small (rabbits, rats, and mice) animal models. This review focuses specifically on the use of the rat to model BPD and summarizes how the model is used in various research studies and the advantages and limitations of this particular model, and it highlights recent therapeutic advances in BPD by using this rat model. hyperoxia; lung development; premature birth BRONCHOPULMONARY DYSPLASIA (BPD) is the most common chronic lung disease of very preterm infants. BPD interrupts lung development and has serious long-term respiratory complications that reach beyond childhood and into adult life (8,25,26,41,53). The multifactorial etiology of BPD has prompted research to investigate the many factors contributing to the pathogenesis of BPD (reviewed in Ref. 38), with the ultimate aim of developing effective therapies to prevent longterm pulmonary sequelae. To investigate the effectiveness of various therapeutic strategies on the development, structure, and function of the lungs, it is important to have animal models that reliably reproduce some of the features observed in very preterm infants developing BPD. To achieve this, known contributing factors of BPD, such as perinatal inflammation, growth restriction, hyperoxia, and mechanical ventilation, have been used in both large and small animals to mimic the BPD-like lung injury. In particular, exposure of neonatal rats to hyperoxia is extensively utilized as a small animal model of experimental BPD. Characterization of the Rat Model of Experimental BPDExposing the immature rat lung to hyperoxic gas through neonatal life closely reproduces the histopathology observed in human infants with BPD. Studies have shown that exposure of the developing rat lung to hyperoxic gas can have detrimental effects, particularly on the structure of the gas-exchanging region (14,30,34,46,62,66). The main overall finding, which is common to each study, is that exposure of the immature lung to hyperoxic gas impairs alveolarization, resulting in fewer and enlarged alveolar air spaces. Pulmonary hypertension, disrupted vascular growth, vascular leakage, accumulation of plasma proteins, extravascular fibrin deposition, increased lung collagen content, increased inflammatory cell influx, and diso...

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“…Many studies have shown that inflammatory markers are elevated in children diagnosed with BPD as neonates. Increased 8-isoprostane levels were detected in the exhaled breath condensate in adolescents born at Յ32 wk of gestation (12). Abnormalities in pulmonary function tests also persist (13,46).…”

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confidence: 88%

Can maternal DHA supplementation offer long-term protection against neonatal hyperoxic lung injury?

Lingappan

Moorthy

2015

American Journal of Physiology-Lung Cellular and Molecular Phys

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Lingappan K, Moorthy B. Can maternal DHA supplementation offer long-term protection against neonatal hyperoxic lung injury?. Am J Physiol Lung Cell Mol Physiol 309: L1383-L1386, 2015. First published September 11, 2015 doi:10.1152/ajplung.00313.2015The effect of adverse perinatal environment (like maternal infection) has long-standing effects on many organ systems, including the respiratory system. Use of maternal nutritional supplements is an exciting therapeutic option that could be used to protect the developing fetus. In a recent issue of the journal, Ali and associates (Ali M, Heyob KM, Velten M, Tipple TE, Rogers LK. Am J Physiol Lung Cell Mol Physiol 309: L441-L448, 2015) specifically look at maternal docosahexaenoic acid (DHA) supplementation and its effect on chronic apoptosis in the lung in a mouse model of perinatal inflammation and postnatal hyperoxia. Strikingly, the authors show that pulmonary apoptosis was augmented even 8 wk after the hyperoxiaexposed mice had been returned to room air. This effect was significantly attenuated in mice that were subjected to maternal dietary DHA supplementation. These findings are novel, significantly advance our understanding of chronic effects of adverse perinatal and neonatal events on the developing lung, and thereby offer novel therapeutic options in the form of maternal dietary supplementation with DHA. This editorial reviews the long-term effects of adverse perinatal environment on postnatal lung development and the protective effects of dietary supplements such as DHA. docosahexaenoic acid; hyperoxia MATERNAL INFLAMMATION DURING pregnancy can occur by intraor extrauterine processes. Maternal infections both systemic (urinary tract infection, periodontitis) and chorioamnionitis have been associated with premature birth (17,27,36,49). Chorioamnionitis leads to fetal lung inflammation in animal models (18,28). The clinical correlation between chorioamnionitis and development of bronchopulmonary dysplasia (BPD) is not strong, with evidence being available both for and against the association (19,41). In animal models, chorioamnionitis induces lung maturation (increase in surfactant proteins) but also causes delayed alveolarization and vascular injury (15, 18). Intra-amniotic lipopolysaccharide (LPS) on embryonic day 15 increases alveolar type II cell number through Toll-like receptor-4 signaling (33). Maternal inflammation can potentially initiate the inflammatory cascade in the fetal lung, which can be further potentiated by postnatal exposures such as hyperoxia (45). Antenatal corticosteroids (maternal ␤-methasone) given to pregnant ewes decrease intrauterine inflammation-induced TGF-␤ signaling in fetal lungs (9). Cao et al. showed that maternal exposure to systemic endotoxin in pregnant rats increases pulmonary inflammation in the pups, altered gene expression of molecules involved in alveologenesis, and delayed morphological maturation (6). Salminen et al. found that, following systemic maternal endotoxin administration, the inflammatory signal is rapidl...

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Evidence of unexpected oxidative stress in airways of adolescents born very pre-term

Cited by 105 publications

References 42 publications

Chronic Lung Disease of Prematurity: Long-Term Respiratory Outcome

Chronic Lung Disease of Prematurity: Long-Term Respiratory Outcome

Animal models of bronchopulmonary dysplasia. The term rat models

Can maternal DHA supplementation offer long-term protection against neonatal hyperoxic lung injury?

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