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Studies on the pathogenic factors of Helicobacter pylori.

幽门螺杆菌致病因素的研究。

基本信息

批准号：
08457089
负责人：
NAKAZAWA Teruko
金额：
$ 4.67万
依托单位：
Yamaguchi University
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (B)
财政年份：
1996
资助国家：
日本
起止时间：
1996 至 1997
项目状态：
已结题

项目摘要

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.

幽门螺杆菌的尿素酶是幽门螺杆菌定植所必需的，也是胃上皮损伤的主要原因。(1)我们分析了尿素酶操纵子的转录产物，发现尿素酶操纵子是在酸性条件下诱导的，是尿素酶激活的必要操纵子之一。我们还确定了尿素酶操纵子的转录起始点，并在ureIE启动子中确定了两个起始点。(2)我们发现幽门螺杆菌对尿素、尿素酶抑制剂、钠离子和碳酸氢根离子具有趋化作用。通过增加粘度，野生型菌株表现出更好的趋化运动，而尿素酶阴性突变株不表现出通过增加粘度来刺激趋化运动。此外，尿素酶抑制剂抑制了野生型菌株的趋化运动，表明尿素酶对该运动是必需的。(3)我们在尿素酶操纵子下游发现了一个与细胞分裂相关的基因CDRA。CarA突变体表现出比野生型菌株更好的生存能力。在大肠杆菌中过量表达的CDRA基因产物抑制宿主细胞的生长。(4)幽门螺杆菌在厌氧条件下呈球状生长。我们分析了幽门螺杆菌中的Sigma因子，发现该细菌不含RpoS。RpoD在指数期和稳定期的表达是恒定的。一个尿素酶阴性突变体在厌氧和低渗透压等胁迫条件下的存活能力低于野生型。(5)建立了双重感染动物模型。幽门螺杆菌在胃中电离后，重组痘苗病毒受到了挑战。幽门螺杆菌感染对细胞毒性T细胞的诱导有抑制作用，导致病毒清除效率低下。