| Project/Area Number |
08457089
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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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 | Yamaguchi University |
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Principal Investigator |
NAKAZAWA Teruko Yamaguchi University School of Medicine, Professor., 医学部, 教授 (40053053)
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| Co-Investigator(Kenkyū-buntansha) |
YOSHIYAMA Hironori Yamaguchi University School of Medicine, Lecturer., 医学部, 講師 (10253147)
SHIRAI Mutsunori Yamaguchi University School of Medicine, Associate Professor, 医学部, 助教授 (20196596)
MIZOTE Tomoko Yamaguchi Prefectural University, Domestic Sciences, Lecturer., 家政学部, 講師 (90145938)
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| Project Period (FY) |
1996 – 1997
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| Project Status |
Completed (Fiscal Year 1997)
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| Budget Amount *help |
¥7,300,000 (Direct Cost: ¥7,300,000)
Fiscal Year 1997: ¥1,400,000 (Direct Cost: ¥1,400,000)
Fiscal Year 1996: ¥5,900,000 (Direct Cost: ¥5,900,000)
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| Keywords | H.pylori infection / urease / coccoid form / sigma factor / cell-division-related gene / CTL induction / transcription analysis / ヘリコバクター・ピロリ感染 / 走化性 / 転写開始点 / ヘリコバクター・ピロリ / 尿素 |
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| Research Abstract |
Urease of Helicobacter pylori is essential for colonization and responsible for gastric epithelial injury.
(1) We analyzed the transcripts of urease operons and found that ureIE,one of the ccessory operons for urease activation, is induced under acidic conditions. We also identified the transcription start sites of urease operons and identified two start sites in the ureIE promoter.
(2) We found chemotactic responses of H.pylori toward urea, urease inhibitors, sodium ion, and bicarbonate ion. By increasing the viscosity, the wild-type strain showed much better chemotactic motility, whereas a urease-negative mutant did not show stimulation of chemotactic motility by increasing the viscosity. In addition, urease inhibitors inhibited the chemotactic motility of the wild-type strain, indicating that urease is essential for the motility.
(3) We found a cell-division-related gene, cdrA,downstream of the urease operon. A carA mutant showed better viability than the wild-type strain. The cdrA gene product overproduced in E.coli inhibited the host cell growth.
(4) H.pylori turned to coccoid forms under anaerobic conditions. We have analyzed the sigma factors in H.pylori and found that the bacterium does not contain RpoS.The expression of RpoD was constant through the exponential and the stationary phase. A urease-negative mutant showed lower viability than the wild type under stress conditions such as anaerobiosis and low osmolarity.
(5) We have established a double infection animal model. After conlonization of H.pylori in the stomach, a recombinant vaccinia virus was challenged. H.pylori infection showed an inhibitory effect on the induction of cytotoxic T cells, resulted in a low efficiency of viral elimination.
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