1990 Fiscal Year Final Research Report Summary
Mediators Released from the Kupffer Cell
| Project/Area Number |
63480206
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| Research Category |
Grant-in-Aid for General Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Gastroenterology
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| Research Institution | Kurume University |
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Principal Investigator |
TANIKAWA Kyuichi Kurume Univ. School of Med. Professor, 医学部, 教授 (10080649)
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| Co-Investigator(Kenkyū-buntansha) |
TANAKA Masatoshi Kurume Univ. School of Med. assistant, 医学部, 助手 (60179786)
NOGUCHI Kazunori Kurume Univ. School of Med. assistant, 医学部, 助手 (40180715)
YOSHIDA Hiroshi Kurume Univ. School of Med. instructor, 医学部, 講師 (60158467)
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| Project Period (FY) |
1988 – 1990
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| Keywords | Kupffer cell / Pit cell / sinusoidal endothelial cell / hepatocyte / endotoxin / TNF / spleen macrophage / alcoholic hepatitis |
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| Research Abstract |
(1) Interaction between the Kupffer cell and hepatocytes or other sinusoidal cells. It has been found in our in vitro studies that the Kupffer cell producing Prostaglandin protects injured hepatocytes, the cell degradates collagens produced by hepatocytes, activated Kupffer cells releasing IL-6 acts to the hepatocyte for the production of CRP, in addition, endotoxin activated Kupffer cells release TNF, however, its amount is much less than that by activated macrophages in the spleen. It was also found that the activation and priloferation of pit cells accompanies with activated Kupffer cells. In chronic ethanol-fed rats, the Kupffer cell showed to have a remarkably depressed endocytotic activity. Isolated and cultured Kupffer cells taken from chronically ethanol-fed rats revealed to be also in depressed endocytotic function. The sinusoidal endothelial cell appeared to be compensatory for the Kupffer cell dysfunction.
(2) Role of the Kupffer cell in pathogenesis of liver injures. In the experimental model of alcoholic hepatitis, endotoxin-induced TNF showed to play an important role in pathogenesis of liver injury. However, splenectomy inhibits liver injuries remarkably, suggesting of an important role of macrophages in the spleen. Similar results were also obtained in Galactosamine-induced liver injury. These data show that functions of Kupffer cells, macrophages in the liver, are different from those of macrophages in the spleen and the Kupffer cell appears to be more protective for the liver and the macrophage in the spleen appears to be more important in pathogenesis of liver injuries.
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