Neonatal hyperoxia contributes additively to cigarette smoke-induced chronic obstructive pulmonary disease changes in adult mice

Research output: Contribution to journalArticle

Abstract

The extent by which early postnatal lung injury contributes to the development of chronic obstructive pulmonary disease (COPD) in the adult is unclear. We hypothesized that exposure to hyperoxia during early postnatal life can augment lung changes caused by adult chronic cigarette smoke(CS) exposure. C57BL/6J mice (1dold) were exposed to hyperoxia (O 2) for 5 days. At 1 month of age, half of the O 2 - exposed mice and half of the control mice were placed in aCS chamber for 6 months. After exposure to CS, mice underwent quasistatic pressure - volume curve and mean chord length measurements; quantification of pro - Sp-c expression; and measurement of lung IL-8/ KC,CXCR2/IL8Ra, TNF-a, and IL-6 mRNA by real-time PCR. Adult mice exposed to O 2+CS had significantly larger chord length measurements (P <0.02) and lung volumes at 35 cm H 2O (P <0.05) compared with all other groups. They also had significantly less pro - Sp-c protein and surfactant protein C mRNA expression (P <0.003). Mice exposed to O 2+CS and CS-only mice had significantly higher lung resistance and longer mean time constants (P <0.01), significantly more inflammatory cells in the bronchoalveolar lavage fluid (P <0.03), and significantly higher levels of lung CXCR2/IL8Rα mRNA compared with mice not exposed to smoke (P <0.02). We conclude that exposure to early postnatal hyperoxia contributed additively to CS-induced COPD changes in adult mice. These results may be relevant to a growing population of preterm children who sustained lung injury in the newborn period and may be exposed to CS in later life.

Original languageEnglish (US)
Pages (from-to)610-616
Number of pages7
JournalAmerican Journal of Respiratory Cell and Molecular Biology
Volume45
Issue number3
DOIs
StatePublished - Sep 1 2011

Fingerprint

Pulmonary diseases
Hyperoxia
Smoke
Tobacco Products
Chronic Obstructive Pulmonary Disease
Lung
Lung Injury
Messenger RNA
Bronchoalveolar Lavage Fluid
Protein C
Interleukin-8
Inbred C57BL Mouse
Surface-Active Agents
Real-Time Polymerase Chain Reaction
Interleukin-6
Newborn Infant
Pressure
Fluids

Keywords

  • Airspace abnormalities
  • Chronic cigarette smoke exposure
  • Chronic obstructive pulmonary disease
  • Early postnatal hyperoxia

ASJC Scopus subject areas

  • Cell Biology
  • Pulmonary and Respiratory Medicine
  • Molecular Biology
  • Clinical Biochemistry

Cite this

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title = "Neonatal hyperoxia contributes additively to cigarette smoke-induced chronic obstructive pulmonary disease changes in adult mice",
abstract = "The extent by which early postnatal lung injury contributes to the development of chronic obstructive pulmonary disease (COPD) in the adult is unclear. We hypothesized that exposure to hyperoxia during early postnatal life can augment lung changes caused by adult chronic cigarette smoke(CS) exposure. C57BL/6J mice (1dold) were exposed to hyperoxia (O 2) for 5 days. At 1 month of age, half of the O 2 - exposed mice and half of the control mice were placed in aCS chamber for 6 months. After exposure to CS, mice underwent quasistatic pressure - volume curve and mean chord length measurements; quantification of pro - Sp-c expression; and measurement of lung IL-8/ KC,CXCR2/IL8Ra, TNF-a, and IL-6 mRNA by real-time PCR. Adult mice exposed to O 2+CS had significantly larger chord length measurements (P <0.02) and lung volumes at 35 cm H 2O (P <0.05) compared with all other groups. They also had significantly less pro - Sp-c protein and surfactant protein C mRNA expression (P <0.003). Mice exposed to O 2+CS and CS-only mice had significantly higher lung resistance and longer mean time constants (P <0.01), significantly more inflammatory cells in the bronchoalveolar lavage fluid (P <0.03), and significantly higher levels of lung CXCR2/IL8Rα mRNA compared with mice not exposed to smoke (P <0.02). We conclude that exposure to early postnatal hyperoxia contributed additively to CS-induced COPD changes in adult mice. These results may be relevant to a growing population of preterm children who sustained lung injury in the newborn period and may be exposed to CS in later life.",
keywords = "Airspace abnormalities, Chronic cigarette smoke exposure, Chronic obstructive pulmonary disease, Early postnatal hyperoxia",
author = "McGrath-Morrow, {Sharon A} and Thomas Lauer and Michael Collaco and Min Yee and Michael O'Reilly and Mitzner, {Wayne A} and Enid Neptune and Wise, {Robert A} and Shyam Biswal",
year = "2011",
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T1 - Neonatal hyperoxia contributes additively to cigarette smoke-induced chronic obstructive pulmonary disease changes in adult mice

AU - McGrath-Morrow, Sharon A

AU - Lauer, Thomas

AU - Collaco, Michael

AU - Yee, Min

AU - O'Reilly, Michael

AU - Mitzner, Wayne A

AU - Neptune, Enid

AU - Wise, Robert A

AU - Biswal, Shyam

PY - 2011/9/1

Y1 - 2011/9/1

N2 - The extent by which early postnatal lung injury contributes to the development of chronic obstructive pulmonary disease (COPD) in the adult is unclear. We hypothesized that exposure to hyperoxia during early postnatal life can augment lung changes caused by adult chronic cigarette smoke(CS) exposure. C57BL/6J mice (1dold) were exposed to hyperoxia (O 2) for 5 days. At 1 month of age, half of the O 2 - exposed mice and half of the control mice were placed in aCS chamber for 6 months. After exposure to CS, mice underwent quasistatic pressure - volume curve and mean chord length measurements; quantification of pro - Sp-c expression; and measurement of lung IL-8/ KC,CXCR2/IL8Ra, TNF-a, and IL-6 mRNA by real-time PCR. Adult mice exposed to O 2+CS had significantly larger chord length measurements (P <0.02) and lung volumes at 35 cm H 2O (P <0.05) compared with all other groups. They also had significantly less pro - Sp-c protein and surfactant protein C mRNA expression (P <0.003). Mice exposed to O 2+CS and CS-only mice had significantly higher lung resistance and longer mean time constants (P <0.01), significantly more inflammatory cells in the bronchoalveolar lavage fluid (P <0.03), and significantly higher levels of lung CXCR2/IL8Rα mRNA compared with mice not exposed to smoke (P <0.02). We conclude that exposure to early postnatal hyperoxia contributed additively to CS-induced COPD changes in adult mice. These results may be relevant to a growing population of preterm children who sustained lung injury in the newborn period and may be exposed to CS in later life.

AB - The extent by which early postnatal lung injury contributes to the development of chronic obstructive pulmonary disease (COPD) in the adult is unclear. We hypothesized that exposure to hyperoxia during early postnatal life can augment lung changes caused by adult chronic cigarette smoke(CS) exposure. C57BL/6J mice (1dold) were exposed to hyperoxia (O 2) for 5 days. At 1 month of age, half of the O 2 - exposed mice and half of the control mice were placed in aCS chamber for 6 months. After exposure to CS, mice underwent quasistatic pressure - volume curve and mean chord length measurements; quantification of pro - Sp-c expression; and measurement of lung IL-8/ KC,CXCR2/IL8Ra, TNF-a, and IL-6 mRNA by real-time PCR. Adult mice exposed to O 2+CS had significantly larger chord length measurements (P <0.02) and lung volumes at 35 cm H 2O (P <0.05) compared with all other groups. They also had significantly less pro - Sp-c protein and surfactant protein C mRNA expression (P <0.003). Mice exposed to O 2+CS and CS-only mice had significantly higher lung resistance and longer mean time constants (P <0.01), significantly more inflammatory cells in the bronchoalveolar lavage fluid (P <0.03), and significantly higher levels of lung CXCR2/IL8Rα mRNA compared with mice not exposed to smoke (P <0.02). We conclude that exposure to early postnatal hyperoxia contributed additively to CS-induced COPD changes in adult mice. These results may be relevant to a growing population of preterm children who sustained lung injury in the newborn period and may be exposed to CS in later life.

KW - Airspace abnormalities

KW - Chronic cigarette smoke exposure

KW - Chronic obstructive pulmonary disease

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