| Project/Area Number |
13670617
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Respiratory organ internal medicine
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| Research Institution | Teikyo University |
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Principal Investigator |
NAKANO Junichi Teikyo University, School of Medicine, Department of medicine, Associate Professor, 医学部, 講師 (20240707)
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| Co-Investigator(Kenkyū-buntansha) |
YAMASHITA Naomi Teikyo University, School of Medicine, Dept of Medicine, Associate Professor, 医学部, 助教授 (20239974)
OHTA Ken Teikyo University, School of Medicine, Dept of Medicine, Professor, 医学部, 教授 (30160500)
金子 富志人 帝京大学, 医学部, 助手 (20328074)
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| Project Period (FY) |
2001 – 2002
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| Project Status |
Completed (Fiscal Year 2002)
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| Budget Amount *help |
¥4,100,000 (Direct Cost: ¥4,100,000)
Fiscal Year 2002: ¥2,000,000 (Direct Cost: ¥2,000,000)
Fiscal Year 2001: ¥2,100,000 (Direct Cost: ¥2,100,000)
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| Keywords | pulmonary fibrosis / mouse / hepatitis C virus / transgenic / cytokine / apoptosis / IL-4 / interstitial pneumonia / 肺繊維症 / HCV / シリカ / トランスジェニック / PDGF / 肝炎 / ウイルス |
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| Research Abstract |
Pathogenesis of IPF (interstitial pulmonary fibrosis) is still unclear despite of its poor prognosis. We hypothesized that HCV, which has been recognized, as one of major pathogen of fibrous change in liver, may play a role in IIP. First, we confirmed patients with IPF have antibody against HCV in a larger population and are more frequently positive in RT-PCR to HCV as compared to controls. In this study we investigated the role of this virus in IPF using the HCV transgenic mouse. In HCV transgenic mouse significantly sever fibrous changes were observed in lung with a small amount of silica such as 8 mg. Pro-inflammatory cytokines such as IGF-1 and TGF-beta increased in the lung in response to silica in a dose dependent manner but no significant differences were observed between transgenic and non-transgenic mouse. On the other hand, HCV transgenic mouse had significantly high expression of mRNA of IL-4 and INF-gamma as compared to controls. These findings proposed that HCV might promote the progression of fibrous changes in lung in response to silica with different profiles of cytokines.
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