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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.
Neonatology. 2010 Jun; 98(1):23-32.N

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 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.

Authors+Show Affiliations

Department of Pediatrics, Dongguk University Ilsan Hospital, Gyeonggi-do, Korea.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

19955834

Citation

Kim, Do-Hyun, et al. "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." Neonatology, vol. 98, no. 1, 2010, pp. 23-32.
Kim DH, Choi CW, Kim EK, et al. 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. Neonatology. 2010;98(1):23-32.
Kim, D. H., Choi, C. W., Kim, E. K., Kim, H. S., Kim, B. I., Choi, J. H., Lee, M. J., & Yang, E. G. (2010). 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. Neonatology, 98(1), 23-32. https://doi.org/10.1159/000263056
Kim DH, et al. 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. Neonatology. 2010;98(1):23-32. PubMed PMID: 19955834.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - 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. AU - Kim,Do-Hyun, AU - Choi,Chang Won, AU - Kim,Ee-Kyung, AU - Kim,Han-Suk, AU - Kim,Beyong Il, AU - Choi,Jung-Hwan, AU - Lee,Myong Jin, AU - Yang,Eun Gyeong, Y1 - 2009/12/02/ PY - 2009/02/02/received PY - 2009/06/10/accepted PY - 2009/12/4/entrez PY - 2009/12/4/pubmed PY - 2010/10/15/medline SP - 23 EP - 32 JF - Neonatology JO - Neonatology VL - 98 IS - 1 N2 - 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. SN - 1661-7819 UR - https://www.unboundmedicine.com/medline/citation/19955834/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_ L2 - https://www.karger.com?DOI=10.1159/000263056 DB - PRIME DP - Unbound Medicine ER -