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.

这个子项目是许多利用资源的研究子项目之一 由NIH/NCRR资助的中心拨款提供。子项目的主要支持 而子项目的主要调查员可能是由其他来源提供的， 包括其它NIH来源。 列出的子项目总成本可能 代表子项目使用的中心基础设施的估计数量， 而不是由NCRR赠款提供给子项目或子项目工作人员的直接资金。 幽门螺杆菌引起胃粘膜炎性浸润，约10%的病例进展为消化性溃疡或胃癌。疾病是由菌株特异性细菌毒力基因和特定宿主反应之间的相互作用引起的，这两者都没有得到很好的理解。用H. pylori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H. pylori发病机制