| Project/Area Number |
15590392
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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 |
Bacteriology (including Mycology)
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| Research Institution | Nagasaki University |
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Principal Investigator |
EHARA Masahiko Nagasaki University, Institute of Tropival Medicine, Research fellow, 熱帯医学研究所, 助手 (70124823)
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| Co-Investigator(Kenkyū-buntansha) |
MORITA Kouichi Nagasaki University, Institute of Tropival Medicine, Professor, 熱帯医学研究所, 教授 (40182240)
AKAIKE Takaaki Kumamoto University, Graduate school of Medicine and Pharmacy, 大学院・医学薬学研究部, 助教授 (20231798)
TODA Takayoshi University of the Rhykyus, Graduate school of Medicine, 医学部, 助教授 (30108295)
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| Project Period (FY) |
2003 – 2004
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| Project Status |
Completed (Fiscal Year 2004)
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| Budget Amount *help |
¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 2004: ¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 2003: ¥2,400,000 (Direct Cost: ¥2,400,000)
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| Keywords | Non-O1 Vibrio cholerae / tissue-invasive / cpxP / signal transduction / multiple drug resistance gene |
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| Research Abstract |
Vibrio cholerae Non-O1 is one of etiologic pathogens causing watery diarrhea as Vibrio cholerae O1 and O139. However there are many reports on extra-intestinal infection of Vibrio cholerae Non-O1 among immunocompromised hosts with liver cirrhosis, malignant tumor as a basic disorder. Many cases are reported among those of liver cirrhosis whose infections with Vibrio cholerae Non-O1 end in sepsis. A half of them is fatal after suffering multiple organ failure. The result of our study to clarify the mechanism of sepsis by Vibrio cholerae Non-O1 is as follows : Each one x 10^8 of Vibrio cholerae Non-O1 (Y strain) was given oally to ddy mouse of 6 weeks of age. Ten hours after administration of bacteria, bacteria were recovered in peripheral blood samples. After 27 hours, bacteria were recovered from all mice in their peripheral blood samples. Between 15-30 hours post administration, all mice were dead. Fatality and incidence was increased depending on the increase of bacterial cell concentration. Through the analyses of samples from abdominal space, potal vein, liver, it was suggested that Vibrio cholerae Non-O1 enter directly into blood vessels through mucous membrane and that they enter into blood stream via portal vein and liver. The concentration of inflammatory cytokines such as L6 and TNFα was also increased depending on the progress of inflammation and sepsis. Histopathologically, degenerative necrosis of liver cells and infarction of spleen were fiequently observed. Our experiment to examine whether Zinoov (a proteinase inhibitor) will suppress sepsis or not, suggests some inhibitory effect. We found cpxP, an inhibitor of signal transduction system, in Non-O1 Vibrio cholerae. Expression of this protein also palys some role in decreasing pathogenicity by suppressing the secretion pathway. Finally, I have to apologize to have changed the reseach theme on the way to "analysis of multi-drug resistance genes of Vibrio cholerae O1"
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