tetano
Editor, Senior Moderator
Am J Physiol Lung Cell Mol Physiol. 2013 Jun 7. [Epub ahead of print]
Neonatal hyperoxia alters the host response to influenza A virus infection in adult mice through multiple pathways.
Buczynski BW, Yee M, Martin KC, Lawrence BP, O'Reilly MA.
Source
1The University of Rochester.
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 (Tg) mice over-expressing 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 over-expression of EC-SOD. However, leukocyte recruitment remained excessive and levels of MCP-1 remained modestly elevated following infection in EC-SOD Tg mice exposed to hyperoxia as neonates. Since 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 KO 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.
KEYWORDS:
lung fibrosis, monocyte chemoattractant protein, neonatal hyperoxia, respiratory viral infection, superoxide dismutase
PMID:
23748535
[PubMed - as supplied by publisher]
http://www.ncbi.nlm.nih.gov/pubmed/23748535
Neonatal hyperoxia alters the host response to influenza A virus infection in adult mice through multiple pathways.
Buczynski BW, Yee M, Martin KC, Lawrence BP, O'Reilly MA.
Source
1The University of Rochester.
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 (Tg) mice over-expressing 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 over-expression of EC-SOD. However, leukocyte recruitment remained excessive and levels of MCP-1 remained modestly elevated following infection in EC-SOD Tg mice exposed to hyperoxia as neonates. Since 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 KO 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.
KEYWORDS:
lung fibrosis, monocyte chemoattractant protein, neonatal hyperoxia, respiratory viral infection, superoxide dismutase
PMID:
23748535
[PubMed - as supplied by publisher]
http://www.ncbi.nlm.nih.gov/pubmed/23748535