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啮齿动物疟疾贫血机制的研究。

Studies on the mechanism of anemia in rodent malaria.

作者信息

Wu Y L, Yu Q, Li W L, Liu E X

出版信息

Proc Chin Acad Med Sci Peking Union Med Coll. 1989;4(2):102-5.

PMID:2798398
Abstract

The underlying cause of anemia is one of the problems to be solved in malaria research. Many factors are involved in reducing the quantity of uninfected red blood cells (RBC) in addition to those infected RBC destroyed by malaria parasites. In the Plasmodium yoelii (P.y.)-mouse model, the amount of [51Cr]-labelled normal mouse RBC destroyed in peripheral blood as well as the quantity phagocytized by spleen cells during acute and chronic infection in vivo is reported in this paper. Our results show that compensatory enlargement of the spleen, which cleans up a large amount of the damaged uninfected RBC, may be the major cause of anemia in chronic malaria infection. In acute malaria infection destruction of uninfected RBC in peripheral circulation is higher than that in normal mice. Neither malaria antigen, mouse autoantibody nor immune complex was detected on the surface of normal RBC from infected mice using indirect immunofluorescence assay (IFA) or [3H]-isoleucine-labelled P.y. antigen (P.y.Ag) in vitro. This suggests that malaria immune complexes do not play an important part in RBC destruction in circulating blood. Since no obvious hemolysis was observed by mixing RBC with P.y. culture supernatant in vitro, it is possible that physical and chemical changes in uninfected RBC induced by malaria metabolites are the prerequisite for their destruction in circulating blood in vivo. Hemolysis occurs due to external stresses, such as those incurred when damaged RBC run into each other in the blood stream or when they change their shape to pass through capillaries.

摘要

贫血的根本原因是疟疾研究中有待解决的问题之一。除了被疟原虫破坏的受感染红细胞外,还有许多因素参与减少未感染红细胞(RBC)的数量。本文报道了约氏疟原虫(P.y.)-小鼠模型中,在急性和慢性体内感染期间外周血中被破坏的[51Cr]标记的正常小鼠红细胞数量以及被脾细胞吞噬的数量。我们的结果表明,脾脏的代偿性肿大清除了大量受损的未感染红细胞,这可能是慢性疟疾感染中贫血的主要原因。在急性疟疾感染中,外周循环中未感染红细胞的破坏高于正常小鼠。使用间接免疫荧光法(IFA)或体外[3H]-异亮氨酸标记的P.y.抗原(P.y.Ag),在感染小鼠的正常红细胞表面未检测到疟原虫抗原、小鼠自身抗体或免疫复合物。这表明疟疾免疫复合物在循环血液中红细胞破坏中不起重要作用。由于在体外将红细胞与P.y.培养上清液混合未观察到明显的溶血现象,因此疟疾代谢产物诱导的未感染红细胞的物理和化学变化可能是其在体内循环血液中被破坏的先决条件。溶血是由于外部压力引起的,例如受损红细胞在血流中相互碰撞或在通过毛细血管时改变形状时所产生的压力。

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Studies on the mechanism of anemia in rodent malaria.啮齿动物疟疾贫血机制的研究。
Proc Chin Acad Med Sci Peking Union Med Coll. 1989;4(2):102-5.
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引用本文的文献

1
Rate of red blood cell destruction varies in different strains of mice infected with Plasmodium berghei-ANKA after chronic exposure.在长期接触感染伯氏疟原虫ANKA株的不同品系小鼠中,红细胞破坏率各不相同。
Malar J. 2009 May 5;8:91. doi: 10.1186/1475-2875-8-91.