Bronchopulmonary Dysplasia in Very Low Birth Weight Subjects and Lung Function in Late Adolescence

Doyle, Lex W.; Faber, B; Callanan, Catherine; Freezer, Nicholas; Ford, Geoffrey; Davis, Noni

doi:10.1542/peds.2005-2522

Cited by 346 publications

(269 citation statements)

References 15 publications

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“…And like children born prematurely who are often rehospitalized when infected with respiratory syncytial virus, 20,21 adult mice exposed to neonatal hyperoxia show increased susceptibility to influenza A virus infection. 33 Since lung function in late adolescents born prematurely might be deteriorating faster than expected, 24 we decided to investigate whether deficits in lung function and structure changed as oxygen-exposed mice aged. We found elevated lung compliance and reduced tissue elastance activity in aged mice, similar to the changes observed at 8 weeks following exposure to neonatal hyperoxia.…”

Section: Discussionmentioning

confidence: 99%

“…20,21 Abnormalities in airflow obstruction and air trapping persist into adolescence. [22][23][24][25][26] Similarly, newborn animals exposed to Ն65% oxygen and recovered in room air develop long-term changes in airway responsiveness and increased lung volumes. [27][28][29][30][31] We previously reported that 8-week-old adult mice exposed to Ն60% oxygen for the first 4 days of life have simplified alveoli attributed to changes in elastin expression and an imbalance in alveolar epithelial type I and II cells.…”

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confidence: 99%

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Neonatal Hyperoxia Causes Pulmonary Vascular Disease and Shortens Life Span in Aging Mice

Yee

White

Awad

et al. 2011

The American Journal of Pathology

111

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Bronchopulmonary dysplasia is a chronic lung disease observed in premature infants requiring oxygen supplementation and ventilation. Although the use of exogenous surfactant and protective ventilation strategies has improved survival, the long-term pulmonary consequences of neonatal hyperoxia are unknown. Here, we investigate whether neonatal hyperoxia alters pulmonary function in aging mice. By 67 weeks of age, mice exposed to 100% oxygen between postnatal days 1 to 4 showed significantly a shortened life span (56.6% survival, n ‫؍‬ 53) compared to siblings exposed to room air as neonates (100% survival, n ‫؍‬ 47). Survivors had increased lung compliance and decreased elastance. There was also right ventricular hypertrophy and pathological evidence for pulmonary hypertension, defined by reduction of the distal microvasculature and the presence of numerous dilated arterioles expressing von Willebrand factor and ␣-smooth muscle actin. Consistent with recent literature implicating bone morphogenetic protein (BMP) signaling in pulmonary vascular disease, BMP receptors and downstream phospho-Smad1/ 5/8 were reduced in lungs of aging mice exposed to neonatal oxygen. BMP signaling alterations were not observed in 8-week-old mice. These data suggest that loss of BMP signaling in aged mice exposed to neonatal oxygen is associated with a shortened life span, pulmonary vascular disease, and associated cardiac failure. People exposed to hyperoxia as neonates may be at increased risk for pulmonary hypertension.

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Neonatal Hyperoxia Causes Pulmonary Vascular Disease and Shortens Life Span in Aging Mice

Yee

White

Awad

et al. 2011

The American Journal of Pathology

111

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show abstract

“…4 Development of lung function from childhood to adulthood is debated and not well understood, and longitudinal studies are few. [9][10][11] Normally, after childhood growth, lung function attains a stable plateau before onset of a physiological age-related decline. 12 The maximum level obtained, the duration of the plateau and the rate of the decline predict if and when obstructive pulmonary disease will occur in later life.…”

Section: Introductionmentioning

confidence: 99%

Lung function after preterm birth: development from mid-childhood to adulthood

Vollsæter

Røksund

Eide

et al. 2013

Thorax

189

148

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“…Fortunately, antenatal steroid administrations to mothers in preterm labor, and the application of exogenous surfactant and mild ventilation strategies to premature babies, have markedly reduced their mortality. Unfortunately, survivors continue to show decreased lung capacity at 5-10 years of age and even as young adolescents (2)(3)(4). Moreover, these children are at increased risk for asthma, infection, and other respiratory diseases, and are often rehospitalized after respiratory infection (5,6).…”

mentioning

confidence: 99%

Neonatal Hyperoxia Enhances the Inflammatory Response in Adult Mice Infected with Influenza A Virus

O’Reilly

Marr

Yee

et al. 2008

Am J Respir Crit Care Med

112

124

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Rationale: Lungs of adult mice exposed to hyperoxia as newborns are simplified and exhibit reduced function much like that observed in people who had bronchopulmonary dysplasia (BPD) as infants. Because survivors of BPD also show increased risk for symptomatic respiratory infections, we investigated how neonatal hyperoxia affected the response of adult mice infected with influenza A virus infection. Objectives: To determine whether neonatal hyperoxia increased the severity of influenza A virus infection in adult mice. Methods: Adult female mice exposed to room air or hyperoxia between Postnatal Days 1 and 4 were infected with a sublethal dose of influenza A virus. Measurements and Main Results: The number of macrophages, neutrophils, and lymphocytes observed in airways of infected mice that had been exposed to hyperoxia as neonates was significantly greater than in infected siblings that had been exposed to room air. Enhanced inflammation correlated with increased levels of monocyte chemotactic protein-1 (CCL2) in lavage fluid, whereas infectionassociated changes in IFN-g, IL-1b, IL-6, tumor necrosis factor-a, KC, granulocyte-macrophage colony-stimulating factor, and macrophage inflammatory protein-1a, and production of virus-specific antibodies, were largely unaffected. Increased mortality of mice exposed to neonatal hyperoxia occurred by Day 14 of infection, and was associated with persistent inflammation and fibrosis. Conclusions: These data suggest that the disruptive effect of hyperoxia on neonatal lung development also reprograms key innate immunoregulatory pathways in the lung, which may contribute to exacerbated pathology and poorer resistance to respiratory viral infections typically seen in people who had BPD.

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Bronchopulmonary Dysplasia in Very Low Birth Weight Subjects and Lung Function in Late Adolescence

Abstract: Subjects of very low birth weight with bronchopulmonary dysplasia in the newborn period have poorer lung function in late adolescence than those without bronchopulmonary dysplasia, and their lung function may be deteriorating at a more rapid rate.

Cited by 346 publications

References 15 publications

Neonatal Hyperoxia Causes Pulmonary Vascular Disease and Shortens Life Span in Aging Mice

Neonatal Hyperoxia Causes Pulmonary Vascular Disease and Shortens Life Span in Aging Mice

Lung function after preterm birth: development from mid-childhood to adulthood

Neonatal Hyperoxia Enhances the Inflammatory Response in Adult Mice Infected with Influenza A Virus

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