| Project/Area Number |
07670678
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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 | Keio University, School of Medicine |
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Principal Investigator |
ISHIZUKA Akitoshi Keio University, School of Medicine, Assistant, 医学部, 助手 (90176181)
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| Co-Investigator(Kenkyū-buntansha) |
KUROSE Iwao Keio University, School of Medicine, Assistant, 医学部, 助手 (50234604)
KANAZAWA Minoru Keio University, School of Medicine, Assistant Professor, 医学部, 専任講師 (80118934)
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| Project Period (FY) |
1995 – 1996
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| Project Status |
Completed (Fiscal Year 1996)
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| Budget Amount *help |
¥2,300,000 (Direct Cost: ¥2,300,000)
Fiscal Year 1996: ¥1,200,000 (Direct Cost: ¥1,200,000)
Fiscal Year 1995: ¥1,100,000 (Direct Cost: ¥1,100,000)
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| Keywords | Acute lung injury / Endotoxin / Mononuclear phagocyte / Reticuloendothelial system / 2-chloroadenosine / Latex particle / Radiation / Cytokine / 肺 / マクロファージ / 単核球系貪食細胞 / 放射線 / 大腸菌 |
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| Research Abstract |
We investigated the contribution of the interaction among organs to the pathogenesis of endotoxin-induced acute lung injury in guinea pigs. We focussed especially on the roles of mononuclear phagocytes in lungs and reticuloendothelial systems. The results of experiments revealed that the reduction of alveolar macrophage function by thoracic radiation could not attenuate acute lung injury. We also estimated the effects of intravenous latex particles which activate reticuloendothelial systems and those of intravenous 2-chloroadenosine (2CA) which selectively attenuates mononuclear phagocyte function. We revealed that endotoxin-induced lung injury occurred in the animals which were administered with latex particle even if they were neutropenic. We, however, observed no injury in guinea pigs which were pretreated with both latex particles and 2CA.The mononuclear phagocytes, both alveolar macrophages and Kuppfer cells in livers, which were recovered from the 2CA-treated animals had attenuated function. These results suggested that acute lung injury could occur in neutropenic animals when the reticuloendothelial systems were activated. Because the suppression of alveolar macrophage function by thoracic radiation could not attenuate lung injury, it has been revealed that alveolar macrophages plays less important roles in the pathogenesis of septic lung injury. In addition, the plasma TNF assay was increased in the latex-treated animals and not in the 2CA-treated animals. We concluded that the reticuloendothelial systems play important roles in the pathogenesis of endotoxin-induced acute lung injury through the production of cytokines or other inflammatory mediators, especially in neutropenic animals.
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