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Published on: January 2, 2013
Iron deficiency influences the course of malaria in Plasmodium berghei infected mice
Saisudha Koka1, Michael Föller, Georg Lamprecht
1Department of Physiology, University of Tübingen, Gmelinstr. 5, D 72076 Tübingen, Germany.
Abstract:
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.
Insights
Iron deficiency accelerates suicidal erythrocyte death, enhancing malaria parasite clearance. This study shows iron deficiency improves outcomes in malaria by increasing infected red blood cell removal.
Area of Science:
- Hematology
- Infectious Diseases
- Parasitology
Background:
- Iron deficiency is linked to accelerated erythrocyte death, indicated by phosphatidylserine exposure.
- The impact of iron deficiency on Plasmodium falciparum infection and erythrocyte survival remains incompletely understood.
Purpose of the Study:
- To investigate if iron deficiency compromises intraerythrocytic Plasmodium growth.
- To determine if iron deficiency enhances infected erythrocyte death, influencing malaria progression.
Main Methods:
- Assessed phosphatidylserine exposure in Plasmodium falciparum-infected human erythrocytes under iron-deficient conditions.
- Evaluated the effect of iron deficiency on in vitro intraerythrocytic Plasmodium growth and infection.
- Studied the clearance of iron-deficient erythrocytes and Plasmodium berghei-infected erythrocytes in mice.
- Monitored parasitemia and survival rates in iron-deficient and control mice infected with P. berghei.
Main Results:
- Phosphatidylserine exposure was significantly increased in iron-deficient, Plasmodium falciparum-infected erythrocytes.
- Iron deficiency impaired in vitro intraerythrocytic Plasmodium growth and infection.
- Iron-deficient erythrocytes showed accelerated clearance from circulation in mice, an effect amplified by P. berghei infection.
- Parasitemia decreased from 54% to 33% in iron-deficient mice, and survival increased from 0% to 20% over 30 days.
Conclusions:
- Iron deficiency favorably influences the course of malaria.
- This beneficial effect is partly attributed to accelerated suicidal death and clearance of infected erythrocytes.
- Iron deficiency may represent a factor modulating malaria severity.
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