No Involvement of Acid Sphingomyelinase in the Secretion of IL-6 from alveolar Macrophages in neonatal rat

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No Involvement of Acid Sphingomyelinase in the Secretion of IL-6 from alveolar Macrophages in neonatal rat

Material type: 博士論文

Author: 伊藤, 智夫ほか

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Publication date: 2014-06-01

Material Format: Digital

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Name of awarding university/degree: 秋田大学,博士（医学）

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Note (General)：: Chronic lung disease (CLD) of the newborn is a major problem in neonatology. Activation of alveolar macrophages has been implicated in the pathogenesi...

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Material Type: 博士論文
Title: No Involvement of Acid Sphingomyelinase in the Secretion of IL-6 from alveolar Macrophages in neonatal rat
Author/Editor: 伊藤, 智夫
Ito, Tomoo
Author Heading: 伊藤, 智夫
Ito, Tomoo
Publication Date: 2014-06-01
Publication Date (W3CDTF): 2014-06-01
Alternative Title: 酸性スフィンゴミエリナーゼはラット肺胞マクロファージからのIL-6 分泌に関与しない
Degree grantor/type: 秋田大学
Date Granted: 2014-03-22
Dissertation Number: 甲第1076号
Degree Type: 博士（医学）
Text Language Code: eng
Subject Heading: chronic lung disease of the newborn
alveolar macrophage
acid sphingomyelinase
Target Audience: 一般
Note (General): Chronic lung disease (CLD) of the newborn is a major problem in neonatology. Activation of alveolar macrophages has been implicated in the pathogenesis of CLD. Acid sphingomyelinase (ASM) responds to diverse cellular stressors, including lipopolysaccharide (LPS) stimulation. Recently, functional inhibitors of acid sphingomyelinase (FIASMAs) have been described as a large group of compounds that inhibit ASM. Here, we used maternal intra-peritoneal LPS injection to model CLD in the infant rat lung. Using this model, we studied ASM activity in the infant rat lung and the effects of FIASMAs on release of interleukin-6 (IL-6) from LPS-stimulated alveolar macrophages. Maternal exposure to LPS non-significantly increased ASM activities in the infant rat lung. FIASMAs significantly decreased ASM activity of LPS-stimulated alveolar macrophages. In addition, some FIASMAs suppressed the release of IL-6 from LPS-stimulated alveolar macrophages during the early response phase. However, FIASMAs did not suppress the release of IL-6 from LPS-stimulated alveolar macrophages. From our study, we could not confirm that ASM activation is responsible for LPS-related pathogenesis of CLD and release of IL-6 from LPS-stimulated alveolar macrophages.
Access Restrictions: インターネット公開
Related Material: http://hdl.handle.net/10295/2502
http://hdl.handle.net/10295/2502
Data Provider (Database): 国立情報学研究所 : 学術機関リポジトリデータベース（IRDB）（機関リポジトリ）
https://irdb.nii.ac.jp
Original Data Provider (Database): 秋田大学 : 秋田大学学術情報リポジトリ