Phytoestrogens and innate immunity in ER deficient mice

ER 缺陷小鼠的植物雌激素和先天免疫

• 批准号: 6575694
• 负责人: Don MARK ESTES
• 金额: $ 6.54万
• 依托单位: UNIVERSITY OF MISSOURI-COLUMBIA
• 依托单位国家: 美国
• 财政年份: 2002
• 资助国家: 美国
• 起止时间: 2002-03-01 至 2003-02-28
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/6575694
• 关键词: Phytoestrogens; innate; immunity; ER; deficient

The goal of this project is to determine the range and mechanism of action of phytoestrogens (genistein, diadzein and soy extracts) on innate immune function via estrogen receptor-dependent and independent pathways. This goal will be accomplished using estrogen receptor deficient (ERKO) severe combined immunodeficient (SCID) mouse models of bacterial inflammation in the gut, liver and spleen. The hypothesis is that estrogen and phytoestrogen signaling is a positive regulator of macrophage and natural killer cell function. Specifically, the project will... 1) Determine the effects of the loss of estrogen receptor alpha signaling on bacterial-induced inflammation. 2) Determine the effects of the loss of estrogen receptor beta signaling on bacterial-induced inflammation. 3) Determine the effects of the loss of estrogen receptors alpha and beta signaling on bacterial induced inflammation. The PI on this project is D. Mark Estes and the co-PI is Criag Franklin. Two consultants on the project are Helen Mullen and Dennis Lubahn. All of these personnel are based at the University of Missouri-Columbia. The sites for the research are the UM-C?s Horticulture and Agroforestery Research Center in New Franklin and the UM-C?s Southwest Research Station in Mt. Vernon.

该项目的目标是确定范围和机制 植物雌激素（染料木黄酮、二黄酮和大豆提取物）对先天性的作用 通过雌激素受体依赖性和独立途径发挥免疫功能。这 目标将通过使用雌激素受体缺陷（ERKO）来实现 联合免疫缺陷（SCID）小鼠细菌炎症模型 肠、肝和脾。假设是雌激素和植物雌激素 信号传导是巨噬细胞和自然杀伤细胞的正调节因子 功能。 具体来说，该项目将... 1) 确定雌激素受体α信号传导丧失对 细菌引起的炎症。 2) 确定雌激素受体β信号传导丧失对 细菌引起的炎症。 3) 确定雌激素受体α和β丧失的影响 细菌引起的炎症的信号传导。 该项目的 PI 是 D. Mark Estes，联合 PI 是 Criag Franklin。二 该项目的顾问是 Helen Mullen 和 Dennis Lubahn。所有这些 人员设在密苏里哥伦比亚大学。网站为 研究是位于新墨西哥大学的园艺和农林业研究中心 富兰克林和位于弗农山的 UM-C 西南研究站。