GENE EXPRESSION DURING H PYLORI-HOST INTERACTION

这个子项目是许多研究子项目中利用 资源由NIH/NCRR资助的中心拨款提供。子项目和 调查员(PI)可能从NIH的另一个来源获得了主要资金， 并因此可以在其他清晰的条目中表示。列出的机构是 该中心不一定是调查人员的机构。 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。

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. 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.