Oxidative insult can induce malaria-protective trait of sickle and fetal erythrocytes

Marek Cyrklaff (), Sirikamol Srismith, Britta Nyboer, Kvetoslava Burda, Angelika Hoffmann, Felix Lasitschka, Sophie Adjalley, Cyrille Bisseye, Jacques Simpore, Ann-Kristin Mueller, Cecilia P. Sanchez, Friedrich Frischknecht and Michael Lanzer ()
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Marek Cyrklaff: Center of Infectious Diseases, Parasitology, Heidelberg University Hospital
Sirikamol Srismith: Center of Infectious Diseases, Parasitology, Heidelberg University Hospital
Britta Nyboer: Center of Infectious Diseases, Parasitology, Heidelberg University Hospital
Kvetoslava Burda: Faculty of Physics and Applied Computer Science, AGH—University of Science and Technology in Kraków
Angelika Hoffmann: Heidelberg University Hospital
Felix Lasitschka: German Centre for Infection Research (DZIF), Partner Site Heidelberg
Sophie Adjalley: European Molecular Biology Laboratory (EMBL)
Cyrille Bisseye: Biomolecular Research Center Pietro Annigoni, University of Ouagadougou
Jacques Simpore: Biomolecular Research Center Pietro Annigoni, University of Ouagadougou
Ann-Kristin Mueller: Center of Infectious Diseases, Parasitology, Heidelberg University Hospital
Cecilia P. Sanchez: Center of Infectious Diseases, Parasitology, Heidelberg University Hospital
Friedrich Frischknecht: Center of Infectious Diseases, Parasitology, Heidelberg University Hospital
Michael Lanzer: Center of Infectious Diseases, Parasitology, Heidelberg University Hospital

Nature Communications, 2016, vol. 7, issue 1, 1-11

Abstract: Abstract Plasmodium falciparum infections can cause severe malaria, but not every infected person develops life-threatening complications. In particular, carriers of the structural haemoglobinopathies S and C and infants are protected from severe disease. Protection is associated with impaired parasite-induced host actin reorganization, required for vesicular trafficking of parasite-encoded adhesins, and reduced cytoadherence of parasitized erythrocytes in the microvasculature. Here we show that aberrant host actin remodelling and the ensuing reduced cytoadherence result from a redox imbalance inherent to haemoglobinopathic and fetal erythrocytes. We further show that a transient oxidative insult to wild-type erythrocytes before infection with P. falciparum induces the phenotypic features associated with the protective trait of haemoglobinopathic and fetal erythrocytes. Moreover, pretreatment of mice with the pro-oxidative nutritional supplement menadione mitigate the development of experimental cerebral malaria. Our results identify redox imbalance as a causative principle of protection from severe malaria, which might inspire host-directed intervention strategies.

Date: 2016
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DOI: 10.1038/ncomms13401

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