Recovery mechanism from LPS-induced lung edema by HGF

2013 Fiscal Year Final Research Report

• Project/Area Number: 23591157
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Respiratory organ internal medicine
• Research Institution: Kyoto Prefectural University of Medicine
• Principal Investigator: IWASAKI YOSHINOBU 京都府立医科大学, 医学(系)研究科(研究院), 准教授 (00203373)
• Co-Investigator(Kenkyū-buntansha): MARUNAKA Yoshinori 京都府立医科大学, 医学研究科, 教授 (00127036) ; NIISATO Naomi 京都府立医科大学, 医学研究科, 准教授 (00237645) ; ARIMOTO Taichiro 京都府立医科大学, 医学研究科, 講師 (30457965) ; UEDA Mikio 京都府立医科大学, 医学研究科, 助教 (40457966) ; KOUNO Yoshihito 京都府立医科大学, 医学研究科, 助教 (90516163)
• Project Period (FY): 2011 – 2013
• Keywords: LPS / lung injury / HGF / 血管透過性 / アポトーシス

Research Abstract

The expression of hepatocyte growth factor (HGF) in pulmonary endothelium was promoted in both gene and protein levels by injecting lipopolysaccaride (LPS) into trachea of mice. Alveolar macrophages isolated from bronchoalveolar lavage fluid were cultured in addition to LPS. IL-1beta and TNF-alpha were introduced from the alveolar macrophages. The expression of HGF in pulmonary endothelium was inhibited in LPS-induced lung injury by adminstering anti-IL-1ß antibody or anti-TNFalpha antibody immediately after injecting LPS into trachea. In LPS-induced lung injury, administration of anti-HGF antibody promoted apoptosis of alveolar epithelium, and pulmonary vascular permeability. It suggested that HGF could play a pivotal role in recovery from LPS-induced lung injury.