1999 Fiscal Year Final Research Report Summary
Study on the role of lymphocytes on organ failure and disturbed host defense mechanism due to infection and stress
Project/Area Number |
09470324
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Research Category |
Grant-in-Aid for Scientific Research (B)
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Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Anesthesiology/Resuscitation studies
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Research Institution | AKITA UNIVERSITY |
Principal Investigator |
INABA Hideo School of Med., Akita Univ., Professor, 医学部, 教授 (60159952)
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Co-Investigator(Kenkyū-buntansha) |
NAKAE Hajime School of Med., Akita Univ., Research Assoc., 医学部, 助手 (10254781)
KUROSAWA Shin School of Med., Tohoku Univ., Research assoc., 医学部, 助手 (60272043)
MOTOYAMA Satoru School of Med., Akita Univ., Research Assoc., 医学部, 助手 (60292372)
TANAKA Hiroyuki School of Med., Akita Univ., Assoc. Prof., 医学部, 助教授 (90266297)
MACHII Masato School of Med., Akita Univ., Research Assoc., 医学部, 助手 (50209467)
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Project Period (FY) |
1997 – 1999
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Keywords | lymphocyte / apoptosis / hydrogen peroxide / hepatocytes / endothelial cells / heat shock protein / bcl-2 / ischemia |
Research Abstract |
Lympocytes may induce acute injuries of the perfused liver when sinusoidal endothelial cell apoptosis is induced by the administration of OK432 or ischemic challenge, and when lymphocytes are activated by concanavalin A. In the schemic liver, hydrogen peroxide derived from hepatocytes induces sisusoidal endothelial cell apoptosis in the midzone of Liver acinus as well as Hsp 72 expression in sinusoidal endothelial cells. An anti-apoptotic protein Bcl-2 is located in the inner membrane and crista of mitochondria in the hepatocytes. Localization of Bcl-2 is unchanged by the ischemic challenge. In a mouse model of severe infection and sepsis induced consequent administrations of Ok432 and lipopolysaccharide, both natural killer and lymphokine-activated killer activities are elevated, but lymphocytes are very sensitive to Fas-mediated apoptosis.
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