Biochem Biophys Res Commun. 2007 Apr 9; [Epub ahead of print]
Iron deficiency influences the course of malaria in Plasmodium berghei
infected mice.
Koka S, Foller M, Lamprecht G, Boini KM, Lang C, Huber SM, Lang F.
Department of Physiology, University of Tubingen, Gmelinstr. 5, D
72076 Tubingen, Germany.
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.
PMID: 17445762 [PubMed - as supplied by publisher]
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