Albright J W, Albright J F
Department of Microbiology, George Washington University School of Medicine, Washington, D.C. 20037.
Infect Immun. 1988 Apr;56(4):831-5. doi: 10.1128/iai.56.4.831-835.1988.
Growth on Trypanosoma musculi in the murine host was limited by the availability of host purines. A portion of the spleen cells of infected mice (many of them granulocytes) displayed high levels of adenosine deaminase (ADA) and purine nucleoside phosphorylase, probably as a compensatory response to extracellular purine deficiency. Injections of adenosine or 2-deoxycoformycin stimulated significant increases in the growth of parasites. 2-Deoxycoformycin treatment also diminished parasite-induced splenomegaly. Treatment of mice with polyethylene glycol-modified ADA, a slowly catabolized form of ADA, had no effect on the course of T. musculi infection, indicating that the parasites can utilize purines other than adenosine. The apparent competition between parasites and host cells for available purines suggests that depletion of extracellular purines should be considered as an approach to treating extracellular trypanosome infections.
鼠宿主中布氏锥虫的生长受到宿主嘌呤可用性的限制。感染小鼠的一部分脾细胞(其中许多是粒细胞)显示出高水平的腺苷脱氨酶(ADA)和嘌呤核苷磷酸化酶,这可能是对细胞外嘌呤缺乏的一种代偿反应。注射腺苷或2-脱氧助间型霉素可刺激寄生虫生长显著增加。2-脱氧助间型霉素治疗还可减轻寄生虫诱导的脾肿大。用聚乙二醇修饰的ADA(一种代谢缓慢的ADA形式)治疗小鼠对布氏锥虫感染进程没有影响,这表明寄生虫可以利用腺苷以外的嘌呤。寄生虫与宿主细胞对可用嘌呤的明显竞争表明,细胞外嘌呤的消耗应被视为治疗细胞外锥虫感染的一种方法。