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Pathophysiological role of Adrenomedullin on the etiology of bronchial asthma and pulmonary fibrosis

Research Project

Project/Area Number 16590737
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeSingle-year Grants
Section一般
Research Field Respiratory organ internal medicine
Research InstitutionThe University of Tokyo

Principal Investigator

YAMAMOTO Hiroshi  The University of Tokyo, Faculty of Medicine, Assistant, 医学部附属病院, 助手 (10361487)

Co-Investigator(Kenkyū-buntansha) NAGASE Takahide  The University of Tokyo, Faculty of Medicine, Professor, 医学部附属病院, 教授 (40208004)
SHINDO Takayuki  Shinshu University, Graduate School of Medicine, Professor, 大学院・医学研究科, 教授 (90345215)
Project Period (FY) 2004 – 2005
Project Status Completed (Fiscal Year 2005)
Budget Amount *help
¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 2005: ¥1,700,000 (Direct Cost: ¥1,700,000)
Fiscal Year 2004: ¥1,800,000 (Direct Cost: ¥1,800,000)
Keywordsbronchial asthma / pulmonary fibrosis / adrenomedullin / 遺伝子改変マウス / 気道過敏症
Research Abstract

Heterozygous Adrenomedullin (AM) gene deficient (AMKO) mice and their litter mate control (Wild type) were applied for this study. OVA-induced murine asthma model mice were introduced ; hence they showed greater responsiveness to Methacholine (MCh) inhalation challenge than the wild type (EC200RL : saline-treated AM^<+/+>, 16.81 ± 2.01mg/ml ; saline-treated AM^<+/->, 16.73± 2.34mg/ml ; OVA-treated AM^<+/+>, 7.95 ± 0.98mg/ml ; OVA-treated AM^<+/->, 2.41 ± 0.63^*mg/ml, respectively, ^*P<0.05 vs. the other groups). Immunoreactive AM in the lung tissue of AMKO mice before and after MCh challenge was significantly lower than the wild type. Tissue AM insufficiency might affect enhance airway responsiveness Morphometrical analysis of the sampled lung tissue sections revealed significant airway narrowing, owing to the trophic change of airway smooth muscle cells and/or the swelling of airway epithelial cells. Peribronchial infiltration by eosinophils, airway hypersecretion or goblet cell hyperplasia, TH1, Th2 cytokines, leukotrienes were assessed, but no significant difference between AMKO mice and wild type mice.

Report

(3 results)
  • 2005 Annual Research Report   Final Research Report Summary
  • 2004 Annual Research Report

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Published: 2004-04-01   Modified: 2016-04-21  

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