ArticleAmerican journal of physiology. Lung cellular and molecular physiology2013
Neonatal hyperoxia alters the host response to influenza A virus infection in adult mice through multiple pathways.
Article in American journal of physiology. Lung cellular and molecular physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 43 citations in OpenAlex.
- Aryl hydrocarbon receptor activation alters emergency hematopoiesis during influenza A virus infection.Toxicological sciences : an official journal of the Society of Toxicology · 2026Article
- Low-dose hyperoxia primes airways for fibrosis in mice after influenza A infection.American journal of physiology. Lung cellular and molecular physiology · 2021Article
- Effect of sex chromosomes versus hormones in neonatal lung injury.JCI insight · 2021Article
- Neonatal hyperoxia inhibits proliferation and survival of atrial cardiomyocytes by suppressing fatty acid synthesis.JCI insight · 2021Article
- Loss of circadian protection against influenza infection in adult mice exposed to hyperoxia as neonates.eLife · 2021Article
- Clocks, Viruses, and Immunity: Lessons for the COVID-19 Pandemic.Journal of biological rhythms · 2021Review
- Neonatal hyperoxia enhances age-dependent expression of SARS-CoV-2 receptors in mice.Scientific reports · 2020Article
- Review
- Early origins of lung disease: towards an interdisciplinary approach.European respiratory review : an official journal of the European Respiratory Society · 2020Review
- Lung SOD3 limits neurovascular reperfusion injury and systemic immune activation following transient global cerebral ischemia.Journal of stroke and cerebrovascular diseases : the official journal of National Stroke Association · 2020Article
- Neonatal hyperoxia enhances age-dependent expression of SARS-CoV-2 receptors in mice.bioRxiv : the preprint server for biology · 2020Article
- Pulmonary mechanics and structural lung development after neonatal hyperoxia in mice.Pediatric research · 2020Article
- Lung-Derived SOD3 Attenuates Neurovascular Injury After Transient Global Cerebral Ischemia.Journal of the American Heart Association · 2019Article
- Long-term pulmonary vascular consequences of perinatal insults.The Journal of physiology · 2019Review
- Neonatal hyperoxia depletes pulmonary vein cardiomyocytes in adult mice via mitochondrial oxidation.American journal of physiology. Lung cellular and molecular physiology · 2018Article
- Lung-Specific Extracellular Superoxide Dismutase Improves Cognition of Adult Mice Exposed to Neonatal Hyperoxia.Frontiers in medicine · 2018Article
- Oxygen-dependent changes in lung development do not affect epithelial infection with influenza A virus.American journal of physiology. Lung cellular and molecular physiology · 2017Article
- Alternative Progenitor Lineages Regenerate the Adult Lung Depleted of Alveolar Epithelial Type 2 Cells.American journal of respiratory cell and molecular biology · 2017Article
- Looking ahead: where to next for animal models of bronchopulmonary dysplasia?Cell and tissue research · 2017Review
- The Oxygen Environment at Birth Specifies the Population of Alveolar Epithelial Stem Cells in the Adult Lung.Stem cells (Dayton, Ohio) · 2016Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Exposing preterm infants or newborn mice to high concentrations of oxygen disrupts lung development and alters the response to respiratory viral infections later in life. Superoxide dismutase (SOD) has been separately shown to mitigate hyperoxia-mediated changes in lung development and attenuate virus-mediated lung inflammation. However, its potential to protect adult mice exposed to hyperoxia as neonates against viral infection is not known. Here, transgenic mice overexpressing extracellular (EC)-SOD in alveolar type II epithelial cells are used to test whether SOD can alleviate the deviant pulmonary response to influenza virus infection in adult mice exposed to hyperoxia as neonates. Fibrotic lung disease, observed following infection in wild-type (WT) mice exposed to hyperoxia as neonates, was prevented by overexpression of EC-SOD. However, leukocyte recruitment remained excessive, and levels of monocyte chemoattractant protein (MCP)-1 remained modestly elevated following infection in EC-SOD Tg mice exposed to hyperoxia as neonates. Because MCP-1 is often associated with pulmonary inflammation and fibrosis, the host response to infection was concurrently evaluated in adult Mcp-1 WT and Mcp-1 knockout mice exposed to neonatal hyperoxia. In contrast to EC-SOD, excessive leukocyte recruitment, but not lung fibrosis, was dependent upon MCP-1. Our findings demonstrate that neonatal hyperoxia alters the inflammatory and fibrotic responses to influenza A virus infection through different pathways. Therefore, these data suggest that multiple therapeutic strategies may be needed to provide complete protection against diseases attributed to prematurity and early life exposure to oxygen.
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