| Project/Area Number |
15591154
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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 |
Embryonic/Neonatal medicine
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| Research Institution | Shinshu University |
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Principal Investigator |
BABA Atsushi Shinshu University, Medicine, 医学部, 助手 (00324252)
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| Co-Investigator(Kenkyū-buntansha) |
YASUI Kozo Shinshu University, Medicine, associate professor, 助教授 (90200493)
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| Project Period (FY) |
2003 – 2004
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| Project Status |
Completed (Fiscal Year 2004)
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| Budget Amount *help |
¥1,800,000 (Direct Cost: ¥1,800,000)
Fiscal Year 2004: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 2003: ¥1,100,000 (Direct Cost: ¥1,100,000)
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| Keywords | Liquid Ventilation / Perfluorocarbon / pulmonary type II cells / IL-8 / lipopolusaccharide / Superoxide dismutase / neurotrophil-mediated inflammation / apoptosis / 細菌性肺炎 / superoxide dismutase / TNF-α / SP-A |
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| Research Abstract |
Perfluorocarbon suppresses lipopolysaccharide and α-toxin induced interleukin-8 release from alveolar epithelial cells.
To determine whether perfiuorocarbon (PFC : FC-84 and perfiubron) can suppress the release of IL-8 from human alveolar epithelial cell line with pulmonary type II (A549) cells stimulated with either lipopolysaccharide (LPS) or α-toxin using an experimental model. The amount of IL-8 released from A549 cells was measured by sandwich-type one step enzyme immunoassay using polyclonal antibodies, and the level of IL-8 mRNA was measured by real-time RT PCR. When stimulated with LPS or α-toxin, A549 cells released more IL-8. After preincubating A549 cells with PFC for 24 hours, PFC was removed, and cells were stimulated with LPS or α-toxin. However, there were no significant differences in the level of IL-8 release with or without preincubation. However, when PFC was administered immediately after LPS or α-toxin stimulation, the level of IL-8 release decreased. Levels of mRNA
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expression with LPS were significantly higher than those without LPS, and levels of mRNA expression with LPS and PFC were significantly lower than those with LPS alone. The present study confirmed that PFC suppresses IL-8 production levels in a human pulmonary alveolar carcinoma cell line with epithelial type II (A549) cells stimulated with LPS or α-toxin.
Superoxide dismutase (SOD) as a potential inhibitory mediator of inflammation via neutrophil apoptosis
Superoxide dismutase (SOD) is supposed to be an effective agent for neutrophil-mediated inflammation in the area of critical medicine. We investigated the involvement of SOD in the regulation of neutrophil apoptosis. Exogenously added SOD effectively induced neutrophil apoptosis, and the fluorescence patterns determined using annexin-V and the 7-AAD were similar to those seen in Fas-mediated neutrophil apoptosis. Neutrophils are short-lived leukocytes that need to be removed safely by apoptosis. The clearance of apoptotic neutrophils from sites of inflammation is a crucial determinant of the resolution of inflammation. Catalase inhibited the neutrophil apoptosis and caspase-3 activation. Spontaneous apoptosis, hydrogen peroxide and anti-Fas antibody-induced apoptosis of neutrophils were accelerated in Down's syndrome patients, in whom the SOD gene is overexpressed. Hydrogen peroxide was thought to be a possible major mediator of ROS-induced neutrophil apoptosis in caspase-dependent manner. Neutrophil apoptosis represents a crucial step in the mechanism governing the resolution of inflammation and has been suggested as a possible target for the control of neutrophil-mediated tissue injury. SOD may be a potential inhibitory mediator of neutrophil-mediated inflammation. Less
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