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Published on: January 16, 2015
Altered small airways in aged mice following neonatal exposure to hyperoxic gas
Megan O'Reilly1, Richard Harding, Foula Sozo
1Department of Anatomy and Developmental Biology, Monash University, Melbourne, Australia.
Insights
Neonatal exposure to high oxygen levels in mice led to lasting changes in airway smooth muscle and lung structure. These alterations in adulthood may impair lung function and increase airway reactivity.
Area of Science:
- Pulmonary Medicine
- Neonatology
- Developmental Biology
Background:
- Supplemental oxygen is crucial for preterm infants but may cause bronchopulmonary dysplasia and long-term lung issues.
- Hyperoxia's impact on alveolarization is known, but its effects on developing conducting airways are unclear.
- Prolonged hyperoxia in immature lungs might alter bronchiolar development, with lifelong consequences.
Purpose of the Study:
- To investigate the long-term effects of neonatal hyperoxia on adult bronchiolar walls.
- To understand how early-life high oxygen exposure influences airway structure and lung function later in life.
Main Methods:
- Neonatal mice inhaled 65% oxygen from birth to day 7, then room air until 10 months.
- Age-matched control mice inhaled room air throughout.
- Small conducting airways (105-310 µm diameter) were analyzed in adulthood.
Main Results:
- Hyperoxia-exposed adult mice had 18% more bronchiolar smooth muscle than controls.
- No significant changes were observed in bronchiolar epithelium or collagen.
- Neonatal hyperoxia led to fewer bronchiolar-alveolar attachments and simplified lung parenchyma.
Conclusions:
- Neonatal hyperoxia causes adult airway remodeling, including increased smooth muscle and reduced attachments.
- These structural changes may lead to impaired lung function and airway hyper-reactivity.
- Early-life hyperoxia presents a potential risk factor for chronic respiratory conditions.
Background:
Supplemental oxygen is necessary in the respiratory support of very preterm infants, but it may contribute to bronchopulmonary dysplasia and an increased risk of poor lung function in later life. It is well established that hyperoxia can inhibit alveolarization, but effects on the developing conducting airways, which are important determinants of lung function, are poorly understood. It is possible that prolonged exposure of the immature lung to hyperoxic gas alters the development of small conducting airways (bronchioles), and that these effects may persist throughout life.
Objectives:
To examine the effects of neonatal inhalation of hyperoxic gas on the bronchiolar walls in adulthood.
Methods:
Neonatal mice (C57BL/6J) born at term inhaled 65% O2 from birth until postnatal day 7; thereafter, they were raised in room air until 10 months postnatal age (P10mo), which is advanced adulthood. Age-matched controls inhaled room air from birth. We investigated small conducting airways with a diameter between 105-310 µm.
Results:
At P10mo, bronchiolar walls of hyperoxia-exposed mice contained ∼18% more smooth muscle than controls (p < 0.05), although there was no effect on bronchiolar epithelium or collagen. Neonatal hyperoxia resulted in significantly fewer bronchiolar-alveolar attachments at P10mo (p < 0.05); this was accompanied by persistent simplification of the lung parenchyma, as indicated by greater mean linear intercept and less parenchymal tissue (p < 0.05).
Conclusions:
Neonatal exposure to hyperoxia induces remodeling of the bronchiolar walls and loss of bronchiolar-alveolar attachments in adulthood, both of which could contribute to impaired lung function and airway hyper-reactivity.
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