Mabbott N, Sternberg J
Department of Zoology, University of Aberdeen, Scotland.
Infect Immun. 1995 Apr;63(4):1563-6. doi: 10.1128/iai.63.4.1563-1566.1995.
Mice infected with Trypanosoma brucei rapidly develop anemia, with the number of circulating erythrocytes reduced by 50% within a week after infection. The present study investigated the relationship between anemia and bone marrow nitric oxide (NO) production. Bone marrow cell populations from T. brucei-infected mice exhibited elevated levels of NO synthase activity which was inhibitable by NG-nitro-L-arginine methyl ester. NO production was found to coincide with suppressed bone marrow T-cell proliferation in response to stimulation with the mitogen concanavalin A both in vitro and in vivo. As this indicated that NO may inhibit proliferation in other cell types, particularly hemopoietic precursors, we examined the role of NO in anemia during trypanosome infection. NO production correlated directly with the development of anemia, and treatment of infected mice with NG-nitro-L-arginine methyl ester in vivo to systemically inhibit NO synthesis led to a significant reduction in the anemia. Thus, elevated NO production in the bone marrow of T. brucei-infected mice is likely to play a significant role in the anemia resulting from T. brucei infection.
感染布氏锥虫的小鼠会迅速出现贫血症状,感染后一周内循环红细胞数量减少50%。本研究调查了贫血与骨髓一氧化氮(NO)生成之间的关系。来自布氏锥虫感染小鼠的骨髓细胞群表现出一氧化氮合酶活性升高,该活性可被NG-硝基-L-精氨酸甲酯抑制。在体外和体内发现,NO生成与骨髓T细胞在有丝分裂原伴刀豆球蛋白A刺激下的增殖抑制相吻合。由于这表明NO可能抑制其他细胞类型的增殖,特别是造血前体细胞,我们研究了NO在锥虫感染期间贫血中的作用。NO生成与贫血的发展直接相关,在体内用NG-硝基-L-精氨酸甲酯治疗感染小鼠以全身抑制NO合成导致贫血显著减轻。因此,布氏锥虫感染小鼠骨髓中NO生成升高可能在布氏锥虫感染引起的贫血中起重要作用。