Neonatal exposure to mild hyperoxia causes persistent increases in oxidative stress and immune cells in the lungs of mice without altering lung structure

Bouch, Sheena; O’Reilly, Megan; Harding, Richard; Sozo, Foula

doi:10.1152/ajplung.00359.2014

Cited by 20 publications

(31 citation statements)

References 75 publications

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confidence: 83%

“…These could predispose the neonates with BPD to the development of respiratory illnesses later in their life. Similar persistent findings into adulthood have been found in neonatal mice exposed to hyperoxia (4,5,34,38,48).Several investigators have noted the protective effects of DHA and its downstream metabolites in various lung diseases. Levels of DHA decrease in premature neonates after birth (24), and this could potentially exacerbate the adverse effects of infection, inflammation, or oxidative stress.…”

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confidence: 76%

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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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confidence: 83%

supporting

confidence: 76%

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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“…Nitrotyrosine is produced in tissue by tyrosine nitration following the formation of peroxynitrite by nitric oxide and the superoxide free radical [ 39 ]. Nitrotyrosine was detected using an established immunohistochemical stain [ 40 ]. In each of the left and right lungs, three and five fields of view of lung parenchyma (free of large conducting airways and major blood vessels) were analyzed at P7d and P56d, respectively.…”

Section: Methodsmentioning

confidence: 99%

Impact of Dietary Tomato Juice on Changes in Pulmonary Oxidative Stress, Inflammation and Structure Induced by Neonatal Hyperoxia in Mice (Mus musculus)

et al. 2016

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Many preterm infants require hyperoxic gas for survival, although it can contribute to lung injury. Experimentally, neonatal hyperoxia leads to persistent alterations in lung structure and increases leukocytes in bronchoalveolar lavage fluid (BALF). These effects of hyperoxia on the lungs are considered to be caused, at least in part, by increased oxidative stress. Our objective was to determine if dietary supplementation with a known source of antioxidants (tomato juice, TJ) could protect the developing lung from injury caused by breathing hyperoxic gas. Neonatal mice (C57BL6/J) breathed either 65% O2 (hyperoxia) or room air from birth until postnatal day 7 (P7d); some underwent necropsy at P7d and others were raised in room air until adulthood (P56d). In subsets of both groups, drinking water was replaced with TJ (diluted 50:50 in water) from late gestation to necropsy. At P7d and P56d, we analyzed total antioxidant capacity (TAC), markers of oxidative stress (nitrotyrosine and heme oxygenase-1 expression), inflammation (interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α) expression), collagen (COL) and smooth muscle in the lungs; we also assessed lung structure. We quantified macrophages in lung tissue (at P7d) and leukocytes in BALF (at P56d). At P7d, TJ increased pulmonary TAC and COL1α1 expression and attenuated the hyperoxia-induced increase in nitrotyrosine and macrophage influx; however, changes in lung structure were not affected. At P56d, TJ increased TAC, decreased oxidative stress and reversed the hyperoxia-induced increase in bronchiolar smooth muscle. Additionally, TJ alone decreased IL-1β expression, but following hyperoxia TJ increased TNF-α expression and did not alter the hyperoxia-induced increase in leukocyte number. We conclude that TJ supplementation during and after neonatal exposure to hyperoxia protects the lung from some but not all aspects of hyperoxia-induced injury, but may also have adverse side-effects. The effects of TJ are likely due to elevation of circulating antioxidant concentrations.

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“…The general characteristics of the study subject can be seen in Table 1. Table 2 shows that preterm infants 28-34 weeks' gestation who developed BPD were 10 (14.7), the median of gestational age in BPD infants was 31.5 (29)(30)(31)(32)(33) and mean birth weight who developed BPD was 1396 (284.9) grams. Half of infants who developed BPD have received antenatal steroids and experience severe respiratory distress.…”

Section: Resultsmentioning

confidence: 99%

“…This chronic inflammation is likely due to the positive feedback cycle due to the production of cell reactive oxygen species (ROS) by inflammatory cells which results in more inflammatory cells in the lung. Exposure to oxygen with a concentration of ≥40% for 7 days can cause an increase in thickening of airway smooth muscle [29,30]. Oxygen toxicity can increase free radical production which can contribute to lung inflammation and remodeling in chronic pulmonary disease.…”

Section: Discussionmentioning

confidence: 99%

Relationship between Serum Interleukin-6 Levels and Bronchopulmonary Dysplasia in Preterm Infants at 28-34 Weeks’ Gestation with Respiratory Distress Syndrome

Alia¹,

Kadi²,

Yuniati³

et al. 2019

AJCMR

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Respiratory distress syndrome (RDS) remains a major cause of mortality and morbidity among preterm infants, especially in developing countries. Up to 40% of those infants who do survive RDS may develop bronchopulmonary dysplasia (BPD). The aim of this study is to find out the relationship between serum IL-6 levels and BPD in preterm infants at 28-34 weeks' gestation with RDS. A cross sectional study was carried out in Department of Child Health Hasan Sadikin General Hospital Bandung in June-September 2018. Serum samples collected within 6-12 hours after birth. Respiratory distress syndrome was diagnosed on the basis of radiographic findings, respiratory distress, and an increasing oxygen requirement. Bronchopulmonary dysplasia was diagnosed based on the requirement of supplemented oxygen by at least 28 days at 36 weeks of post menstrual age (PMA). Serum IL-6 levels were measured using enzyme-linked immunosorbent assay (ELISA). Data was analyzed using logistic regression. Sixty-eight neonates were studied. Ten developed BPD and 58 were not. Based on logistic regression showed that an increase of 1 pg/mL of serum IL-6 levels from the normal values examined at 6-12 hours after birth in preterm infants at 28-34 weeks' gestation with RDS would increase log odds of BDP by 0.005 (p = 0.031) after adjustment for confounding factors of birth weight and gestational age. Increased in serum IL-6 levels within 6-12 hours after birth in preterm infants at 28-34 weeks' gestation with RDS was associated with an increased risk of BPD.

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Neonatal exposure to mild hyperoxia causes persistent increases in oxidative stress and immune cells in the lungs of mice without altering lung structure

Cited by 20 publications

References 75 publications

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

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

Impact of Dietary Tomato Juice on Changes in Pulmonary Oxidative Stress, Inflammation and Structure Induced by Neonatal Hyperoxia in Mice (Mus musculus)

Relationship between Serum Interleukin-6 Levels and Bronchopulmonary Dysplasia in Preterm Infants at 28-34 Weeks’ Gestation with Respiratory Distress Syndrome

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