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Published on: May 10, 2022
Increased Plasmodium chabaudi malaria mortality in mice with nutritional iron deficiency can be reduced by short-term
Filip C Castberg1,2, Lasse Maretty1, Trine Staalsoe1
1Centre for Medical Parasitology, Department of Clinical Microbiology, Copenhagen University Hospital (Rigshospitalet), Copenhagen, Denmark.
Insights
Nutritional iron deficiency increases mortality in mice infected with malaria. Carefully timed iron supplementation can partially offset this increased risk, suggesting a potential therapeutic strategy.
Area of Science:
- Nutritional immunology
- Malaria research
- Hematology
Background:
- Iron deficiency is the most common nutrient deficiency globally, impacting child development.
- Its role in malaria is debated, as it may offer protection but also worsen outcomes.
- This controversy complicates iron deficiency interventions in malaria-endemic regions.
Purpose of the Study:
- To investigate the impact of nutritional iron deficiency on malaria outcomes in a mouse model.
- To evaluate the effect of intravenous iron supplementation on malaria severity.
- To analyze iron status markers and tissue pathology in malaria-infected mice.
Main Methods:
- Assessed the clinical outcome of Plasmodium chabaudi AS infection in iron-deficient A/J mice.
- Administered intravenous ferric carboxymaltose before and after infection.
- Measured plasma hepcidin and fibroblast growth factor 23, and examined liver and spleen pathology.
Main Results:
- Iron deficiency correlated with higher mortality rates in P. chabaudi malaria.
- Short-term iron supplementation mitigated some of the increased mortality.
- Moribund mice exhibited low hepcidin and high fibroblast growth factor 23 levels.
- Splenic extramedullary hematopoiesis was observed in all infected mice; iron supplementation led to visible intracellular iron stores.
Conclusions:
- Nutritional iron deficiency exacerbates malaria mortality in this model.
- Judicious, short-term iron supplementation shows promise as an adjunct therapy.
- This suggests a potential alternative to blood transfusions for severe anemia in pediatric malaria.
Background:
Iron deficiency is the most widespread nutrient deficiency and an important cause of developmental impairment in children. However, some studies have indicated that iron deficiency can also protect against malaria, which is a leading cause of childhood morbidity and mortality in large parts of the world. This has rendered interventions against iron deficiency in malaria-endemic areas controversial.
Methods:
The effect of nutritional iron deficiency on the clinical outcome of Plasmodium chabaudi AS infection in A/J mice and the impact of intravenous iron supplementation with ferric carboxymaltose were studied before and after parasite infection. Plasma levels of the iron status markers hepcidin and fibroblast growth factor 23 were measured in animals surviving and succumbing to malaria, and accompanying tissue pathology in the liver and the spleen was assessed.
Results:
Nutritional iron deficiency was associated with increased mortality from P. chabaudi malaria. This increased mortality could be partially offset by carefully timed, short-duration adjunctive iron supplementation. Moribund animals were characterized by low levels of hepcidin and high levels of fibroblast growth factor 23. All infected mice had extramedullary splenic haematopoiesis, and iron-supplemented mice had visually detectable intracellular iron stores.
Conclusions:
Blood transfusions are the only currently available means to correct severe anaemia in children with malaria. The potential of carefully timed, short-duration adjunctive iron supplementation as a safe alternative should be considered.
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