Iron deficiency influences the course of malaria in Plasmodium berghei infected mice

被引:52
作者
Koka, Saisudha
Foeller, Michael
Lamprecht, Georg
Boini, Krishna M.
Lang, Camelia
Huber, Stephan M.
Lang, Florian
机构
[1] Univ Tubingen, Dept Physiol, D-72076 Tubingen, Germany
[2] Univ Tubingen, Dept Med 1, Tubingen, Germany
关键词
eryptosis; phosphatidylserine; parasitemia; cell volume; anemia;
D O I
10.1016/j.bbrc.2007.03.175
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Iron deficiency accelerates suicidal erythrocyte death, which is evident from phosphatidylserine exposure. The present study explored whether iron deficiency compromises intraerythrocytic growth of Plasmodium and enhances death of infected erythrocytes thus influencing the course of malaria. As a result, phosphatidylserine exposure is increased in Plasmodium falciparum infected human erythrocytes, an effect significantly more marked in iron deficiency. Moreover, iron deficiency impairs in vitro intraerythrocytic growth and infection of erythrocytes. In mice, iron-deficient erythrocytes are more rapidly cleared from circulating blood, an effect increased by infection with Plasmodium berghei. Parasitemia in P. berghei infected mice was significantly decreased (from 54% to 33% of circulating erythrocytes 20 days after infection) and mouse survival significantly enhanced (from 0% to 20% 30 days after infection) in iron-deficient mice. In conclusion, iron deficiency favourably influences the course of malaria, an effect partially due to accelerated suicidal death and subsequent clearance of infected erythrocytes. (c) 2007 Elsevier Inc. All rights reserved.
引用
收藏
页码:608 / 614
页数:7
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