Project/Area Number |
04304032
|
Research Category |
Grant-in-Aid for Co-operative Research (A)
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Allocation Type | Single-year Grants |
Research Field |
細菌学
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Research Institution | Jichi Medical School |
Principal Investigator |
NAKANO Masayasu Jichi Medical School, Dept.Microbiol., Professor, 医学部, 教授 (70048958)
|
Co-Investigator(Kenkyū-buntansha) |
HONDA Takeshi Osaka Univ., Research Institute for Microbial Deseases, Professor, 微生物病研究所, 教授 (60029808)
TAKEDA Yoshifumi Kyoto University Sch.Medicine, Professor, 医学部, 教授 (30029772)
YOKOCHI Takashi Aichi Medical Univ., Dept.Microbiol., Professor, 医学部, 教授 (20126915)
MITUYAMA Masao Niigata University Sch.Medicine, Professor, 医学部, 教授 (10117260)
NODA Masatoshi Chiba University School of Medicine, Professor, 医学部, 教授 (60164703)
中村 信一 金沢大学, 医学部, 教授 (90019620)
木下 タロウ 大阪大学, 微生物病研究所, 教授 (10153165)
|
Project Period (FY) |
1992 – 1993
|
Project Status |
Completed (Fiscal Year 1993)
|
Budget Amount *help |
¥15,000,000 (Direct Cost: ¥15,000,000)
Fiscal Year 1993: ¥6,000,000 (Direct Cost: ¥6,000,000)
Fiscal Year 1992: ¥9,000,000 (Direct Cost: ¥9,000,000)
|
Keywords | Bacterial toxins / Endotoxin / Lipopolysaccharide / Exotoxin / Cytotoxic toxins / 細胞傷害 / LPS / 蛋白毒素 / GPIアンカー |
Research Abstract |
1. Research for intracellular toxins (endotoxins and microcystins) : (A) LPS (endotoxins) : LPS-induced TNF-alpha production by the murine peritoneal macrophages is dependent on protein kinase Cbeta, but the production of IL-1beta depends mainly on calmodulin.adrenocorticoides participate in LPS-induced murine thymocyte apoptosis. P.gingivalis LPS activates tyrosine kinases in LPS-nonresponsive C3H/HeJ B cells. (B) Damage of rat liver cells by microcystin is partialy dependent on the cytotoxic mediators produced by non-parenchymal liver cells. 2. Research for exotoxins : No.167 (glutamic acid) and no.170 (arginine) amino acids from N-terminal of A subunit are essential for the cytotoxic activity of Vero toxin. Protease, furin, in target cell membrane is essential for activation of diphthelia toxin. Hemolytic toxin, TDH, of V.parahemolytics phosphorylates 25kDa protein in red blood cells after binding the receptors. The enhancer (ARFs) and suppressor (ARIs) of cholera toxin were purified from target cells. The mechnisms on penetration of ST1 toxin through inner membrane of E.coil was clarified. The receptor gene for ST toxin was transfected to COS7 cells and the products were analyzed. C.difficile produces a red blood cell agglutinin which is different from toxin A.The release of neurotransmitter by tetanus toxin depends on calmodulin. The listerolysin O-producing strains of L.monocytogenes only can induce inflamatory cytokine mRNAs in infected hosts and endow them the cellular immunity. Protease SH produced by A-group streptococci may be participated in septic shock. Super-antigens may cause scalet fever, symptomes of Yersinia and Kawasaki disease.
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