title: Differential responses in the lungs of newborn mouse pups exposed to 85% or >95% oxygen.
abstract: Premature infants often develop serious clinical complications associated with respiratory failure and hyperoxic lung injury that includes lung inflammation and alterations in lung development. The goal of these studies is to test the hypothesis that there are differences in the course of lung injury in newborn mice exposed to 85% or >95% oxygen that provide models to address the differential effects of oxidation and inflammation. Our results indicate differences between the 85% and >95% O2 exposure groups by day 14 in weight gain and lung alveolarization. Inflammation, assessed by neutrophil counts, was observed in both hyperoxia groups by day 3 but was dramatically greater in the >95% O2-exposed groups by day 14 and associated with greater developmental deficits. Cytoplasmic phospholipase A2, cyclooxygenase-2, and 5-lipoxygenase levels were elevated but no patterns of differences were observed between exposure groups. Prostaglandins D2, E2, and F2alpha were increased in the tissues from mouse pups exposed to >95% O2 at 7 d indicating a differential expression of cyclooxygenase-2 products. Our data indicate that there are differences in the models of 85% or >95% O2 exposure and these differences may provide mechanistic insights into hyperoxic lung injury in an immature system.
authors.affiliation: The Center for Perinatal Research, The Research Institute at Nationwide Children's Hospital, Department of Pediatrics, Ohio State University, Columbus, Ohio 43205, USA. rogersl@ccri.net
authors.forename: Lynette K
authors.initials: LK
authors.lastname: Rogers
authors.forename: Trent E
authors.initials: TE
authors.lastname: Tipple
authors.forename: Leif D
authors.initials: LD
authors.lastname: Nelin
authors.forename: Stephen E
authors.initials: SE
authors.lastname: Welty
mesh_terms: D055371:Acute Lung Injury / Q000139:chemically induced / Q000201:enzymology / Q000276:immunology / Q000473:pathology*; D000818:Animals; D000831:Animals, Newborn; D001094:Arachidonate 5-Lipoxygenase / Q000378:metabolism; D001835:Body Weight; D051546:Cyclooxygenase 2 / Q000378:metabolism; D004195:Disease Models, Animal; D054513:Group IV Phospholipases A2 / Q000378:metabolism; D018496:Hyperoxia / Q000139:chemically induced / Q000201:enzymology / Q000276:immunology / Q000473:pathology*; D008168:Lung / Q000201:enzymology / Q000276:immunology / Q000473:pathology*; D051379:Mice; D008809:Mice, Inbred C3H; D020556:Neutrophil Infiltration; D010100:Oxygen; D011453:Prostaglandins / Q000378:metabolism; D011650:Pulmonary Alveoli / Q000473:pathology; D013929:Thromboxane B2 / Q000378:metabolism; D013997:Time Factors; D015854:Up-Regulation
chemical_list: D011453:Prostaglandins; D013929:Thromboxane B2; D001094:Arachidonate 5-Lipoxygenase; C077623:Ptgs2 protein, mouse; D051546:Cyclooxygenase 2; D054513:Group IV Phospholipases A2; D010100:Oxygen