{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,6]],"date-time":"2026-03-06T16:35:20Z","timestamp":1772814920205,"version":"3.50.1"},"reference-count":35,"publisher":"Oxford University Press (OUP)","issue":"3","license":[{"start":{"date-parts":[[2011,9,1]],"date-time":"2011-09-01T00:00:00Z","timestamp":1314835200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2011,9,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>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 (1 d old) were exposed to hyperoxia (O2) for 5 days. At 1 month of age, half of the O2\u2013exposed mice and half of the control mice were placed in a CS chamber for 6 months. After exposure to CS, mice underwent quasi-static pressure\u2013volume curve and mean chord length measurements; quantification of pro\u2013Sp-c expression; and measurement of lung IL-8\/ KC, CXCR2\/IL8R\u03b1, TNF-\u03b1, and IL-6 mRNA by real-time PCR. Adult mice exposed to O2+CS had significantly larger chord length measurements (P &amp;lt; 0.02) and lung volumes at 35 cm H2O (P &amp;lt; 0.05) compared with all other groups. They also had significantly less pro\u2013Sp-c protein and surfactant protein C mRNA expression (P &amp;lt; 0.003). Mice exposed to O2+CS and CS-only mice had significantly higher lung resistance and longer mean time constants (P &amp;lt; 0.01), significantly more inflammatory cells in the bronchoalveolar lavage fluid (P &amp;lt; 0.03), and significantly higher levels of lung CXCR2\/IL8R\u03b1 mRNA compared with mice not exposed to smoke (P &amp;lt; 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.<\/jats:p>","DOI":"10.1165\/rcmb.2010-0259oc","type":"journal-article","created":{"date-parts":[[2011,1,14]],"date-time":"2011-01-14T22:02:17Z","timestamp":1295042537000},"page":"610-616","source":"Crossref","is-referenced-by-count":22,"title":["Neonatal Hyperoxia Contributes Additively to Cigarette Smoke\u2013Induced Chronic Obstructive Pulmonary Disease Changes in Adult Mice"],"prefix":"10.1093","volume":"45","author":[{"given":"Sharon A.","family":"McGrath-Morrow","sequence":"first","affiliation":[{"name":"Department of Pediatric Pulmonary, Johns Hopkins School of Medicine, Baltimore Maryland"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Thomas","family":"Lauer","sequence":"additional","affiliation":[{"name":"Department of Pediatric Pulmonary, Johns Hopkins School of Medicine, Baltimore Maryland"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"J. 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