Kim, Do-Hyun Choi, Chang Won Kim, Ee-Kyung Kim, Han-Suk Kim, Beyong Il Choi, Jung-Hwan Lee, Myong Jin Yang, Eun Gyeong 2024-01-20T19:03:58Z 2024-01-20T19:03:58Z 2021-09-05 2010-06 1661-7800 https://pubs.kist.re.kr/handle/201004/131384 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 beta(1) (TGF-beta(1)), 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-beta 1. Conclusions: The priming effect of intra-amniotic LPS on hyperoxic lung injury may be associated with IL-6 elevation in the lungs. Copyright (C) 2009 S. Karger AG, Basel English KARGER FIBROBLAST GROWTH-FACTOR PRETERM INFANTS INFLAMMATION ENDOTOXIN DISEASE PREMATURITY VENTILATION NEUTROPHILS BIRTH 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 Article 10.1159/000263056 1 NEONATOLOGY, v.98, no.1, pp.23 - 32 NEONATOLOGY 98 1 23 32 scie scopus 000274315300004 2-s2.0-70849129152 Pediatrics Pediatrics Article FIBROBLAST GROWTH-FACTOR PRETERM INFANTS INFLAMMATION ENDOTOXIN DISEASE PREMATURITY VENTILATION NEUTROPHILS BIRTH Alveolarization Bronchopulmonary dysplasia Inflammation Interleukin-6