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: 7715600
• 负责人: JAY V. SOLNICK
• 金额: $ 5.42万
• 依托单位: UNIVERSITY OF CALIFORNIA AT DAVIS
• 依托单位国家: 美国
• 财政年份: 2008
• 资助国家: 美国
• 起止时间: 2008-05-01 至 2009-04-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7715600
• 关键词: Computer Retrieval of Information on Scientific Projects Database; Coupled; Disease; Funding; Gastric mucosa; Gastritis; Gene Expression; Genes; Genetic Transcription; Genomics; Grant; Helicobacter pylori; Human; Immune response; Immunization; Infection; Inflammatory Infiltrate; Institution; Macaca; Macaca mulatta; Modeling; Outcome; Pathogenesis; Peptic Ulcer; Personal Satisfaction; Pylorus; Research; Research Personnel; Resources; Source; Technology; United States National Institutes of Health; Urease; Vaccines; Virulence; Work; aluminum sulfate; functional genomics; in vivo; malignant stomach neoplasm; novel; pathogen

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. Objective: 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. Rapid progress in genomics and gene expression technologies makes it possible to use the macaque model to study the H. pylori host-pathogen interaction by in vivo analysis of gene expression. We propose to extend our work in the rhesus model of H. pylori into an analysis of bacterial (Specific Aim 1) and host (Specific Aim 2) gene expression during experimental infection. Since the host immune response is increasingly recognized as a critical variable in the outcome of infection, we will also study host gene transcription after immunization with urease coupled with either CpG or alum adjuvant, in order to promote a Th1 or Th2 immune response, respectively (Specific Aim 3). These studies will provide a functional genomic understanding of the H. pylori host-pathogen relationship that may have implications for novel treatment or vaccine strategies.

该副本是利用众多研究子项目之一 由NIH/NCRR资助的中心赠款提供的资源。子弹和 调查员（PI）可能已经从其他NIH来源获得了主要资金， 因此可以在其他清晰的条目中代表。列出的机构是 对于中心，这不一定是调查员的机构。 目的：幽门螺杆菌在胃粘膜中引起炎症性浸润性，在大约10％的病例中发展为消化性溃疡疾病或胃癌。疾病是由于菌株特异性细菌毒力基因与特定宿主反应之间的相互作用而产生的，疾病均未得到充分理解。由于用幽门螺杆菌对恒河猕猴进行实验接种会导致胃炎密切模仿人类感染，因此该模型为我们提供了一个独特的机会，可以进一步了解我们对幽门螺杆菌发病机理的理解。基因组学和基因表达技术的快速发展使使用猕猴模型通过体内基因表达分析研究幽门螺杆菌宿主 - 病原体相互作用。我们建议将幽门螺杆菌模型的工作扩展到实验感染期间细菌（特定目标1）和宿主（特定目标2）基因表达的分析。 由于宿主的免疫反应越来越多地被认为是感染结果中的关键变量，因此我们还将在免疫后与脲酶与CpG或Alum辅助剂相结合后研究宿主基因转录，以分别促进Th1或Th2免疫反应（特定AIM 3）。这些研究将对幽门螺杆菌宿主 - 病原体关系的功能性基因组理解，这可能对新的治疗或疫苗策略具有影响。