MT VET COBRE PROJECT 1: HOST-PATHOGEN COMMUNICATION IN TOXOPLASMA

MT VET COBRE 项目 1：弓形虫中的宿主-病原体通讯

• 批准号: 7721025
• 负责人: JAY R RADKE
• 金额: $ 17.99万
• 依托单位: MONTANA STATE UNIVERSITY - BOZEMAN
• 依托单位国家: 美国
• 财政年份: 2008
• 资助国家: 美国
• 起止时间: 2008-08-01 至 2009-07-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7721025
• 关键词: Acquired Immunodeficiency Syndrome; Cells; Clinical; Communication; Computer Retrieval of Information on Scientific Projects Database; Cyst; Development; Disease; Environment; Funding; Gene Expression; Grant; Infection; Institution; Modeling; Molecular; Organ Transplantation; Parasites; Pathogenesis; Patients; Proteins; Pyrroles; Research; Research Personnel; Resources; Signal Pathway; Source; Tissues; Toxoplasma; Toxoplasma gondii; United States National Institutes of Health; chemotherapy; human subject; pathogen; prenatal

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. Toxoplasma gondii infects 1.5 million human subjects annually and is dangerous to the unborn, to patients undergoing chemotherapy or organ transplant, and to people with AIDS. Bradyzoite development in the intermediate host leads to permanent infection and underlies the pathogenesis of clinical disease in these clinical contexts. Dr. Radke's lab has determined that selected tri-substituted pyrroles will alter gene expression in various model host cells to induce developmentally competent tachyzoite strains to differentiate and form bradyzoite tissues cysts. They suspect new host cell gene expression modulates specific pathways that signal parasites to differentiate. The ability to experimentally alter the host cell to initiate bradyzoite development provides new experimental strategies to study pathogenesis. The identification of host cell proteins that define the molecular environment conducive to bradyzoite differentiation may provide targets for the treatment of this infection.

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。 弓形虫每年感染150万人，对未出生的人、接受化疗或器官移植的患者以及艾滋病患者都是危险的。慢殖子在中间宿主中的发育导致永久感染，并在这些临床背景下形成临床疾病的发病机制。拉德克博士的实验室已经确定，选定的三取代吡咯将改变各种模型宿主细胞中的基因表达，以诱导具有发育能力的速殖子菌株分化并形成缓体组织包囊。他们怀疑，新的宿主细胞基因表达调节了特定的途径，发出寄生虫分化的信号。通过实验改变宿主细胞以启动缓殖体发育的能力为研究发病机制提供了新的实验策略。鉴定宿主细胞蛋白，确定有利于缓殖子分化的分子环境，可能为这种感染的治疗提供靶点。