| Project/Area Number |
03671115
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
Laboratory medicine
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| Research Institution | The Jikei University School of Medicine |
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Principal Investigator |
KUROSAKA Kosei The Jikei University School of Medicine Department of Medicine Professor, 医学部, 教授 (40056502)
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| Co-Investigator(Kenkyū-buntansha) |
OHMAYU Suzuko The Jikei University School of Medicine Department of Medicine Instructor, 医学部, 助手 (70203932)
HOSHINA Sadayori The Jikei University School of Medicine Department of Medicine Lecturer, 医学部, 講師 (30119846)
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| Project Period (FY) |
1991 – 1993
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| Project Status |
Completed (Fiscal Year 1993)
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| Budget Amount *help |
¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 1993: ¥300,000 (Direct Cost: ¥300,000)
Fiscal Year 1992: ¥900,000 (Direct Cost: ¥900,000)
Fiscal Year 1991: ¥900,000 (Direct Cost: ¥900,000)
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| Keywords | coagulase negative staphylococci / opportunistic infection / bacteriophage / apotransferrin / apolipoprotein / protein kinase / heat shock protein / second messenger / 日和見感染症 / ファージ型別 / 燐酸転移酵素活性 / 熱シヨック蛋白 / 生化学プロファイル / DNase陽性株 / S.epidermidis / 細胞内信号伝達系 / コアグラ-ゼ陰性ブドウ球菌 / 生化学性状プロファイル / ファ-ジ型別 |
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| Research Abstract |
Coagulase negative staphylococci is thought to be difficult organism to distinguish causative agent from just contaminant of the normal flora.
We focused S.epidermidis to chose its virulent factors in opportunistic infection.
First, we could differentiate S.epidermidis by bacteriophage to three groups, in which group II and group nontypable indicated the clinical strains, meanwhile all the groups could be isolated from normal flora.
Second, clinical strains showed slight growth in normal hnman serum instead of normal floral strains were diminished in the normal sera. We isolated apotransferrin and apolipoprotein as antibacterial agent in sera, to stress bacterial growth. The clinical strains resist to grow more strongly in sera of immunocompromised host as opportunistic pathogen.
Third, we demonstrated Ca^<2+>, phospholipid dependent protein kinase which substrates serine, threonine of heat-shock protein from S.epidermidis and E.coli. This phosphokinase showed homology to sevenless kinase of Drosophila, suggests its role as second messenger in the S.epidermidis to resist to grow against antibacterial agent in sera.
We think these mechanisms against serum strss of bacteria could be a candidate of virulence factor of these opportunistic pathogens.
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