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

这个子项目是许多研究子项目中的一个 由NIH/NCRR资助的中心赠款提供的资源。子项目和 研究者（PI）可能从另一个NIH来源获得了主要资金， 因此可以在其他CRISP条目中表示。所列机构为 研究中心，而研究中心不一定是研究者所在的机构。 弓形虫每年感染150万人，对胎儿、接受化疗或器官移植的患者以及艾滋病患者都有危险。 中间宿主中的缓殖子发育导致永久性感染，并成为这些临床背景下临床疾病发病机制的基础。 Radke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，以诱导发育能力的速殖子菌株分化并形成缓殖子组织包囊。 他们怀疑新的宿主细胞基因表达调节特定的信号途径，寄生虫分化。 通过实验改变宿主细胞以启动缓殖子发育的能力为研究发病机制提供了新的实验策略。 确定的宿主细胞蛋白，定义的分子环境，有利于缓殖子分化可能提供治疗这种感染的目标。

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.