| Project/Area Number |
08671431
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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 |
Digestive surgery
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| Research Institution | Nagoya University |
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Principal Investigator |
KAMIYA Junichi School of Medicine Nagoya University Associate Professor, 医学部, 講師 (70194975)
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| Co-Investigator(Kenkyū-buntansha) |
YOSHIKAI Yasunobu School of Medicine Professor, 医学部, 教授 (90158402)
KANAI Michio School of Medicine Assistant Professor, 医学部, 助手 (50242871)
MIYACHI Masahiko Aichi Medical University Assosoate Professor, 講師 (80242874)
NAGINO Masato School of Medicine, Assosiate Professor, 医学部, 講師 (20237564)
NIMURA Yuji School of Medicine, Professor, 医学部, 教授 (80126888)
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| Project Period (FY) |
1996 – 1997
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| Project Status |
Completed (Fiscal Year 1997)
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| Budget Amount *help |
¥2,200,000 (Direct Cost: ¥2,200,000)
Fiscal Year 1997: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 1996: ¥1,700,000 (Direct Cost: ¥1,700,000)
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| Keywords | bacterial infection / liver cell injury / cytokines / heat shok protein / endotoxin / TNF-alpha tumor necrosis factor / interleukin-12 / interleukin-10 / 肝不全 / 生体防御機構 / 腫瘍懐死因子-α / 熱ショックタンパク質 / DibutyrylサイクリックAMP / インターロイキン10 / マクロファージ / Salmonella / monoclonal antibody / TNFα / apoptosis |
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| Research Abstract |
Recently extensive liver resection has been performed for treatment of hepatobiliary malignancies. However, bacterial infection sometimes results in posthepatectomy liver failure which is a major cause of operative death. We have investigated mechanisms of hepatocyte injury caused by various cytokines and heat shock protein (Hsp) which derived from bacterial infection. Kupffer cells (macrophages) induced by lipopolysaccharide produce tumor necrosis factor (TNF)-alfa and interleukin (IL)-12 which are main triggers for hepatocyte injury. Dibutyryl cyclic adenosine monophosphate (cAMP) andprostaglandin E2 induce intracellular cAMP and inhibit hepatocyte injury. We propose an explanation that increased intracellular cAMP induces IL-b and Hsp 70 which inhibit TNF-alfa and TL-12. However, these cytokines (TNF-alfa, IL-12 and interferon gamma) also activate macrophages to exclude bacteria. So, treatments which induce intracellular cAMP may also indirectly inhibit bacterial-resistant properties. In order to prevent hepatic failure caused by bacterial infection, we should make a method of hepatocyte protection which preserve bacteria-fighting mechanisms.
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