Innate immune responses and chronic inflammatory lung diseases

2015 Fiscal Year Final Research Report

• Project/Area Number: 25293192
• Research Category: Grant-in-Aid for Scientific Research (B)
• Allocation Type: Partial Multi-year Fund
• Section: 一般
• Research Field: Respiratory organ internal medicine
• Research Institution: Kagoshima University
• Principal Investigator: Inoue Hiromasa 鹿児島大学, 医歯学域医学系, 教授 (30264039)
• Co-Investigator(Kenkyū-buntansha): YAMASAKI Sho 九州大学, 生体医学研究所, 教授 (40312946) ; INOSHIMA Ichiro 九州大学, 医学研究院, 助教 (90380419) ; SAMUKAWA Takuya 鹿児島大学, 医歯学域医学部・歯学部附属病院, 助教 (10363623)
• Co-Investigator(Renkei-kenkyūsha): MARUYAMA Ikuro 鹿児島大学, 医歯学総合研究科, 特任教授 (20082282) ; KUBO Masato 東京理科大学, 生命医科学研究所, 教授 (40277281)
• Research Collaborator: WATANABE Masaki 鹿児島大学, 医歯学総合研究科, 特任助教 (90398298)
• Project Period (FY): 2013-04-01 – 2016-03-31
• Keywords: 自然免疫 / 呼吸器 / 炎症性肺疾患

Outline of Final Research Achievements

We studied the role of innate immune responses and its interaction with adaptive immune pathways in chronic inflammatory lung diseases and chronic pulmonary infections.
We found that high mobility group box 1 (HMGB1), one of the damage-associated molecular patterns, is released into the extracellular space during the early stage of an animal model of pulmonary arterial hypertension and contributes to the development of pulmonary arterial hypertension. Dectin-2 contributes to host immunity against mycobacterial infection through the recognition of mannose-capped lipoarabinomannan. Serum B cell activating factor (BAFF) levels were higher in the patients with connective tissue diseases-associated interstitial lung diseases compared to healthy subjects and the patients with idiopathic pulmonary fibrosis or idiopathic nonspecific interstitial pneumonia.

Free Research Field

医歯薬学