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Original Paper

Association of Increased Pulmonary Interleukin-6 with the Priming Effect of Intra-Amniotic Lipopolysaccharide on Hyperoxic Lung Injury in a Rat Model of Bronchopulmonary Dysplasia

Kim D.-H.a, c · Choi C.W.b, c · Kim E.-K.c · Kim H.-S.c · Kim B.I.b, c · Choi J.-H.c · Lee M.J.d · Yang E.G.d

Author affiliations

aDepartment of Pediatrics, Dongguk University Ilsan Hospital, and bClinical Research Institute, Seoul National University Bundang Hospital, Gyeonggi-do, cDepartment of Pediatrics, Seoul National University College of Medicine, and dLife Sciences Research Division, Korea Institute of Science and Technology, Seoul, Korea

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Neonatology 2010;98:23–32

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Article / Publication Details

First-Page Preview
Abstract of Original Paper

Received: February 02, 2009
Accepted: June 10, 2009
Published online: December 02, 2009
Issue release date: June 2010

Number of Print Pages: 10
Number of Figures: 4
Number of Tables: 1

ISSN: 1661-7800 (Print)
eISSN: 1661-7819 (Online)

For additional information: https://www.karger.com/NEO

Abstract

Background: The authors previously demonstrated the priming effect of intra-amniotic lipopolysaccharide (LPS) on hyperoxic lung injury in a rat model of bronchopulmonary dysplasia (BPD). Objectives: To investigate the mechanism underlying this priming effect by determining biochemical profiles in a rat model of BPD. Methods: The rat model involved intra-amniotic LPS administration and postnatal hyperoxia (85%). The mRNA expressions of interleukin-6 (IL-6), vascular endothelial growth factor (VEGF), VEGF receptor-2 (VEGFR-2), basic fibroblast growth factor (bFGF), and transforming growth factor β1 (TGF-β1), as well as the protein levels of IL-6, VEGF, and protein carbonyl in lung tissue were compared between the LPS plus hyperoxia, the LPS only, the hyperoxia only, and the control groups. Results: Morphometric analysis of lung tissues demonstrated that alveolarization was significantly inhibited only in the LPS plus hyperoxia group. IL-6 protein levels and its mRNA expression in the lungs were significantly increased only in the LPS plus hyperoxia group. Neither LPS nor hyperoxia increased IL-6 in the lungs independently. bFGF mRNA expression was significantly decreased in the LPS-treated groups. VEGF protein levels were significantly reduced by hyperoxia, whereas protein carbonyl levels were increased by intra-amniotic LPS or hyperoxia. No additional significant change to VEGF or protein carbonyl levels was produced by intra-amniotic LPS or hyperoxia. There were no significant differences in the mRNA expressions of VEGF, VEGFR-2, and TGF-β1. Conclusions: The priming effect of intra-amniotic LPS on hyperoxic lung injury may be associated with IL-6 elevation in the lungs.

© 2009 S. Karger AG, Basel


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Article / Publication Details

First-Page Preview
Abstract of Original Paper

Received: February 02, 2009
Accepted: June 10, 2009
Published online: December 02, 2009
Issue release date: June 2010

Number of Print Pages: 10
Number of Figures: 4
Number of Tables: 1

ISSN: 1661-7800 (Print)
eISSN: 1661-7819 (Online)

For additional information: https://www.karger.com/NEO


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