GENE EXPRESSION DURING H PYLORI-HOST INTERACTION

幽门螺杆菌-宿主相互作用期间的基因表达

• 批准号: 8357261
• 负责人: JAY V. SOLNICK
• 金额: $ 5.04万
• 依托单位: UNIVERSITY OF CALIFORNIA AT DAVIS
• 依托单位国家: 美国
• 财政年份: 2011
• 资助国家: 美国
• 起止时间: 2011-05-01 至 2012-04-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/8357261
• 关键词: California; Disease; Funding; Gastric mucosa; Gastritis; Gene Expression; Genes; Grant; Helicobacter pylori; Human; Immune response; Infection; Inflammatory Infiltrate; Macaca mulatta; Modeling; National Center for Research Resources; Pathogenesis; Peptic Ulcer; Primates; Principal Investigator; Research; Research Infrastructure; Resources; Source; United States National Institutes of Health; Virulence; cost; malignant stomach neoplasm

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. Primary support for the subproject and the subproject's principal investigator may have been provided by other sources, including other NIH sources. The Total Cost listed for the subproject likely represents the estimated amount of Center infrastructure utilized by the subproject, not direct funding provided by the NCRR grant to the subproject or subproject staff. Helicobacter pylori causes an inflammatory infiltrate in gastric mucosa that in about 10% of cases progresses to peptic ulcer disease or gastric cancer. Disease results from an interaction between strain-specific bacterial virulence genes and the particular host response, neither of which is well understood. Since experimental inoculation of rhesus macaques with H. pylori causes gastritis that closely mimics human infection, this model provides a unique opportunity to further our understanding of H. pylori pathogenesis.

这个子项目是利用资源的许多研究子项目之一。 由NIH/NCRR资助的中心拨款提供。对子项目的主要支持 子项目的首席调查员可能是由其他来源提供的， 包括美国国立卫生研究院的其他来源。为子项目列出的总成本可能 表示该子项目使用的中心基础设施的估计数量， 不是由NCRR赠款提供给次级项目或次级项目工作人员的直接资金。 幽门螺杆菌在胃粘膜引起炎性浸润，大约10%的病例进展为消化性溃疡疾病或胃癌。疾病是由菌株特定的细菌毒力基因和特定的宿主反应之间的相互作用造成的，这两者都不是很好的理解。由于恒河猴实验性接种幽门螺杆菌引起的胃炎与人类感染非常相似，该模型为我们进一步了解幽门螺杆菌的发病机制提供了一个独特的机会。