Seattle Biomedical Research Institute, Seattle, Washington 98109.
Seattle Biomedical Research Institute, Seattle, Washington 98109; Department of Global Health, University of Washington, Seattle, Washington 98195.
J Biol Chem. 2013 May 17;288(20):14256-14263. doi: 10.1074/jbc.M112.447441. Epub 2013 Apr 2.
Trypanosoma brucei sp. causes human African trypanosomiasis (HAT; African sleeping sickness). The parasites initially proliferate in the hemolymphatic system and then invade the central nervous system, which is lethal if not treated. New drugs are needed for HAT because the approved drugs are few, toxic, and difficult to administer, and drug resistance is spreading. We showed by RNAi knockdown that T. brucei isoleucyl-tRNA synthetase is essential for the parasites in vitro and in vivo in a mouse model of infection. By structure prediction and experimental analysis, we also identified small molecules that inhibit recombinant isoleucyl-tRNA synthetase and that are lethal to the parasites in vitro and highly selective compared with mammalian cells. One of these molecules acts as a competitive inhibitor of the enzyme and cures mice of the infection. Because members of this class of molecules are known to cross the blood-brain barrier in humans and to be tolerated, they may be attractive as leading candidates for drug development for HAT.
布氏锥虫属引起人类非洲锥虫病(HAT;非洲昏睡病)。寄生虫最初在血液淋巴系统中增殖,然后侵入中枢神经系统,如果不治疗则具有致命性。由于现有的药物数量少、毒性大且难以管理,而且耐药性正在传播,因此需要新的药物来治疗 HAT。我们通过 RNAi 敲低实验表明,布氏锥虫异亮氨酸 tRNA 合成酶在体外和感染小鼠模型的体内对寄生虫是必需的。通过结构预测和实验分析,我们还鉴定了一些小分子,它们可以抑制重组异亮氨酸 tRNA 合成酶,在体外对寄生虫具有致死性,并且与哺乳动物细胞相比具有高度选择性。其中一种分子作为该酶的竞争性抑制剂,可治愈感染的小鼠。由于这类分子已知可穿过血脑屏障并被人体耐受,因此它们可能成为治疗 HAT 的有吸引力的候选药物。