Cloning of a Hookworm Excretory-Secretory Protein
钩虫排泄蛋白的克隆
基本信息
- 批准号:6622327
- 负责人:
- 金额:$ 4.81万
- 依托单位:
- 依托单位国家:美国
- 项目类别:
- 财政年份:2002
- 资助国家:美国
- 起止时间:2002-03-10 至
- 项目状态:未结题
- 来源:
- 关键词:Nematoda active immunization anemia animal extract antibody complementary DNA disease /disorder model gene expression hamsters host organism interaction immunity immunocytochemistry laboratory rabbit molecular cloning northern blottings parasitic gastrointestinal disorder parasitism passive immunization pathologic process polymerase chain reaction protein biosynthesis protein purification protein structure function recombinant proteins secretory protein western blottings
项目摘要
DESCRIPTION: provided by the candidate): Hookworms are a major global public
health problem, infecting over a billion people worldwide. Blood feeding adult
hookworms are a leading cause of anemia and malnutrition in developing
countries, extracting a particularly devastating toll on children and women of
childbearing age. Adult worms secrete numerous factors at the site of
attachment in the intestine that are likely to contribute to disease
pathogenesis. Accordingly, the initial aims of this project are the molecular
cloning, expression, and characterization of AcES-1, a novel
excretory-secretory protein which ahs been isolated from the human hookworm
Ancylostoma ceylanicum. Using an animal model of hookworm infection the role of
AcES-1 in pathogenesis will then be examined using active and passive
immunization techniques. Aside from shedding light in the nature of the
host-parasite interaction, study of factors such as AcES-1 may ultimately yield
novel targets for immunological or pharmacological intervention to reduce the
burden of hookworm disease.
描述:由候选人提供):钩虫是一种主要的全球公共
健康问题,感染了全球超过十亿人。吸血成虫
钩虫是发展中国家贫血和营养不良的主要原因
这些国家的儿童和妇女遭受了特别惨重的损失,
生育年龄蠕虫在分泌部位分泌多种因子,
肠内附着物可能导致疾病
发病机制因此,该项目的最初目标是分子
新型AcES-1的克隆、表达和表征
从人钩虫中分离出的一种排泄分泌蛋白
锡兰钩虫使用钩虫感染的动物模型,
AcES-1的发病机制,然后将检查使用主动和被动
免疫技术。除了揭示了
宿主-寄生虫相互作用,对AcES-1等因子的研究可能最终产生
免疫学或药理学干预的新靶点,
钩虫病的负担。
项目成果
期刊论文数量(0)
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会议论文数量(0)
专利数量(0)
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RICHARD D BUNGIRO的其他文献
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