Abstract

Membrane electrochemical potential is a feature of the molecular profile of the cell membrane and the two-dimensional arrangement of its charge-bearing molecules. Plasmodium species, the causative agents of malaria, are intracellular parasites that remodel host erythrocytes by expressing their own proteins on erythrocyte membranes. Although various aspects of the modifications made to the host erythrocyte membrane have been extensively studied in some human Plasmodium species (such as Plasmodium falciparum), details of the structural and molecular biological modifications made to host erythrocytes by nonhuman Plasmodium parasites have not been studied. We employed zeta potential analysis of erythrocytes parasitized by P. chabaudi, a nonhuman Plasmodium parasite. From these measurements, we found that the surface potential shift was more negative for P. chabaudi-infected erythrocytes than for P. falciparum-infected erythrocytes. However, electron microscopic analysis of the surface of P. chabaudi-infected erythrocytes did not reveal any modifications as compared with nonparasitized erythrocytes. These results suggest that differences in the membrane modifications found herein represent unique attributes related to the pathogenesis profiles of the two different malaria parasite species in different host animals and that these features have been acquired through parasite adaptations acquired over long evolutionary time periods.

Highlights

  • Malaria, a serious infectious disease in humans, is caused by protozoan parasites of the genus Plasmodium

  • We investigated the physicochemical aspects of the erythrocyte membrane in terms of the structural modifications induced by infection with the rodent malaria parasite P. chabaudi and we describe here the host cell modifications that are characteristic of this parasite species

  • A smooth surface in the P. chabaudi-infected erythrocytes was quite obvious in comparison with P. falciparum-infected erythrocytes, which form knob-like structures on the erythrocyte surface [44,45,46,47], unlike the very smooth surface topography of uninfected human erythrocytes observed in the scanning electron (Figure 1(e)) and transmission electron (Figure 1(f)) micrographs

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Summary

Introduction

A serious infectious disease in humans, is caused by protozoan parasites of the genus Plasmodium. Infections with Plasmodium induce cellular and molecular alterations to erythrocytes, such as cell adhesion [2,3,4,5], Band 3 clustering [6], erythrocyte-IgG association [7], increased hemichrome attachment to the host erythrocyte membrane [6], increased cell permeability [8], changes in erythrocyte rigidity [9,10,11], and, with certain parasite species, the appearance of knob-like structures on the cell surface [12,13,14,15,16]. These features of human malaria parasites are reported to vary in different hosts but are not known for all parasite species and hosts at the erythrocyte level

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