权益分类	功能权益	普通用户	{{item.name}}会员
{{category.name}}	{{benefitItem.name}}

A Study on the Role of Protease Produced by Vibrio cholerae non-01 in the Pathogenic Mechanism of Sepsis.

霍乱弧菌non-01产生的蛋白酶在脓毒症致病机制中作用的研究。

基本信息

批准号：
10670262
负责人：
ICHINOSE Yoshio
金额：
$ 1.73万
依托单位：
Institute of Tropical Medicine, Nagasaki University
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
1998
资助国家：
日本
起止时间：
1998 至 2000
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-10670262/
关键词：
Vibrio cholerae non-01 metalloprotease invasive mechanism Vibrio cholerae invasive factor

项目摘要

There are many reports on the cases of Vibrio cholerae infection which may extend to extra-intestinal organs. It can result in sepsis and multiple organ failure especially in immunocompromised hosts. It is then considered that a metalloprotease produced by Vibrio cholerae may be involved in its invasive mechanisms of vibrios into tissues or vessels. Because it is a permeability factor to activate kinin cascade and an activating factor of a matrix metalloprotease produced by leukocytes migrating in the inflammatory lesion. We were then trying to develop an animal model of sepsis due to Vibrio cholerae 019 to elucidate the invasive mechanisms of Vibrio cholerae. The results obtained through the study on the role of metalloprotease in pathogenic mechanisms of Vibrio cholerae and histopathological findings in sepsis model are as follows ;(1)Improvement of purification method of choleraprotease.(2)Establishment of assay system of choleraprotease using immunoblotting with ECL kit.(3)Analysis of nicking site of cholera toxin by choleraprotease.(4)Development of mouse sepsis model using Vibrio cholerae 019.(5)Involvement of choleraprotease in the pathogenic mechanism of sepsis.(6)Involvement of iNOS in the pathogenic mechanism of sepsis.

有许多关于霍乱弧菌感染可扩展到肠外器官的病例报告。它可导致脓毒症和多器官功能衰竭，特别是在免疫功能低下的宿主中。因此认为霍乱弧菌产生的金属蛋白酶可能参与了其侵入组织或血管的机制。因为它是激活激肽级联反应的渗透性因子，也是炎性病变中白细胞迁移产生的基质金属蛋白酶的激活因子。因此，我们试图建立一种由霍乱弧菌019引起的脓毒症动物模型，以阐明霍乱弧菌的侵袭机制。通过对金属蛋白酶在霍乱弧菌致病机制中的作用及脓毒症模型的组织病理学研究，取得了如下结果：（1）霍乱蛋白酶纯化方法的改进。（2）用ECL试剂盒建立了霍乱蛋白酶免疫印迹检测体系。（3）霍乱毒素切口位点的霍乱蛋白酶分析。（4）用霍乱弧菌019建立小鼠脓毒症模型。（5）胆固醇蛋白酶参与脓毒症的发病机制。（6）诱导型一氧化氮合酶参与脓毒症的发病机制。