Onset of hepatic erythropoiesis after malarial infection in mice

被引:16
作者
Halder, RC
Abe, T
Mannoor, MK
Morshed, SRM
Ariyasinghe, A
Watanabe, H
Kawamura, H
Sekikawa, H
Hamada, H
Nishiyama, Y
Ishikawa, H
Toba, K
Abo, T [1 ]
机构
[1] Niigata Univ, Sch Med, Dept Immunol, Niigata 9518510, Japan
[2] Keio Univ, Sch Med, Dept Microbiol, Tokyo 1608582, Japan
[3] Niigata Univ, Sch Med, Dept Internal Med 1, Niigata 9518510, Japan
关键词
Plasmodium yoelii; liver; erythropoiesis; merozoites;
D O I
10.1016/S1383-5769(03)00029-1
中图分类号
R38 [医学寄生虫学]; Q [生物科学];
学科分类号
07 ; 0710 ; 09 ; 100103 ;
摘要
Plasmodium yoelii-infected erythrocytes were injected into mice with or without 6.5 Gy irradiation. This irradiation suppressed erythropoiesis and induced severe immunosuppression. However, these mice showed a rather delayed infection, suggesting that fresh erythrocytes may become malarial targets. In other words, malarial infection did not persist without newly generated erythrocytes in mice. We then examined erythropoiesis in the liver and bone marrow of mice with malaria. Surprisingly, erythropoiesis began in the liver. At this time, the serum level of erythropoietin (EPO) was prominently elevated and the EPO mRNA also became detectable in the kidney. Many clusters of red blood cells appeared de novo in the parenchymal space of the liver. These results revealed that malarial infection had a potential to induce the onset of hepatic erythropoiesis in mice. (C) 2003 Elsevier Ireland Ltd. All rights reserved.
引用
收藏
页码:259 / 268
页数:10
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