Heat Shock Proteins and Helicobacter Pylori Pathogenesis

热休克蛋白和幽门螺杆菌发病机制

基本信息

批准号：
6744168
负责人：
EVELYN A. KURT-JONES
金额：
$ 25.76万
依托单位：
UNIV OF MASSACHUSETTS MED SCH WORCESTER
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：
2002-05-15 至 2007-04-30
项目状态：
已结题

来源：
https://reporter.nih.gov/project-details/6744168
关键词：
CD14 molecule Helicobacter bacteria infection mechanism bacterial proteins bactericidal immunity carcinogenesis gastritis genetically modified animals heat shock proteins human tissue inflammation laboratory mouse pathologic process peptic ulcer stomach neoplasms tissue /cell culture toll like receptor

项目摘要

DESCRIPTION (provided by applicant): Helicobacter pylori infection causes gastritis, peptic ulcer disease, gastric atrophy and gastric cancer. The World Health Organization has classified H. pylori as a Class I carcinogen. In animal models, the progression of H. pylori disease from superficial gastritis to gastric cancer is related to the severity of the host inflammatory response. The identification of H. pylori components and host factors that contribute to the inflammatory response may lead to important insights into the mechanism of peptic ulcer disease and/or gastric malignancy. Heat shock proteins are potent activators of inflammatory cytokine production. Heat shock proteins produced by bacteria and endogenous heat shock proteins produced by damaged tissue cell accumulate in foci of infection and inflammation. Our recent data indicate that Toll-like receptors and CD14 are important in the innate immune response to bacterial heat shock proteins. In this proposal we will investigate the role of Toll-like receptors in the recognition of bacterial heat shock proteins and in the control of bacterial infection and inflammation. Specifically, we will use in vitro and in vivo approaches to investigate the role of heat shock proteins in H. pylori infection and pathogenesis and development of tumors.

描述（由申请人提供）：幽门螺杆菌感染的原因胃炎、消化性溃疡病、胃萎缩和胃癌。世界健康组织已将幽门螺杆菌列为 I 类致癌物。在动物中模型中，幽门螺杆菌疾病从浅表性胃炎发展为胃癌的发生与宿主炎症反应的严重程度有关。幽门螺杆菌成分和宿主因子的鉴定有助于炎症反应可能会导致对机制的重要见解消化性溃疡病和/或胃恶性肿瘤。热休克蛋白是有效的炎症细胞因子产生的激活剂。产生的热休克蛋白细菌和受损组织细胞产生的内源性热休克蛋白积聚在感染和炎症病灶中。我们最近的数据表明 Toll 样受体和 CD14 在先天免疫反应中很重要细菌热休克蛋白。在本提案中，我们将研究以下角色的作用： Toll 样受体识别细菌热休克蛋白和控制细菌感染和炎症。具体来说，我们将使用研究热休克蛋白作用的体外和体内方法幽门螺杆菌感染与肿瘤的发病机制和发展。