The deformability of red blood cells parasitized by Plasmodium falciparum and P. vivax.

Red blood cells (RBCs) must deform considerably during their multiple passages through the microvasculature and the sinusoids of the spleen. RBCs infected with Plasmodium falciparum (Pf-IRBCs) become increasingly rigid as they mature but avoid splenic clearance by sequestering in venules and capillaries. In contrast, RBCs infected with P. vivax (Pv-IRBCs) do not sequester. We compared the effects of P. vivax and P. falciparum infection on RBC deformability in a laminar shear flow system. Pf-IRBCs became more rigid as the parasite matured, but equivalent maturation of Pv-IRBCs resulted in a doubling of flexibility. Coincidentally, the IRBC surface area increased from 56.7+/-1.3 microm2 to 74.7+/-0.6 microm2 to 90.9+/-1.1 microm2 in ring-, trophozoite-, and schizont-stage Pv-IRBCs, respectively, whereas Pf-IRBCs did not increase in size. P. vivax increases the deformability of IRBCs and thereby avoids splenic entrapment.

[1]  R. Coppel,et al.  The malaria-infected red blood cell: Structural and functional changes , 2001, Advances in Parasitology.

[2]  S. Usami,et al.  A simplified method for culture of endothelial cells and analysis of adhesion of blood cells under conditions of flow. , 1993, Microvascular research.

[3]  L. Miller,et al.  Caveola--vesicle complexes in the plasmalemma of erythrocytes infected by Plasmodium vivax and P cynomolgi. Unique structures related to Schüffner's dots. , 1975, The American journal of pathology.

[4]  K. Silamut,et al.  Ex-vivo short-term culture and developmental assessment of Plasmodium vivax. , 2001, Transactions of the Royal Society of Tropical Medicine and Hygiene.

[5]  I. Gluzman,et al.  Plasmodium falciparum maturation abolishes physiologic red cell deformability. , 1984, Science.

[6]  R. Stocker,et al.  Oxidative stress and the redox status of malaria-infected erythrocytes. , 1990, Blood cells.

[7]  R. Coppel,et al.  An alternative to serum for cultivation of Plasmodium falciparum in vitro. , 1997, Transactions of the Royal Society of Tropical Medicine and Hygiene.

[8]  R. J. Howard.  Malarial proteins at the membrane of Plasmodium falciparum-infected erythrocytes and their involvement in cytoadherence to endothelial cells. , 1988, Progress in allergy.

[9]  A. Cowman,et al.  Contribution of parasite proteins to altered mechanical properties of malaria-infected red blood cells. , 2002, Blood.

[10]  G. Nash,et al.  Abnormalities in the mechanical properties of red blood cells caused by Plasmodium falciparum. , 1989, Blood.

[11]  R. Coppel,et al.  A recombinant peptide based on Pf EMP‐1 blocks and reverses adhesion of malaria‐infected red blood cells to CD36 under flow , 1998, Molecular microbiology.

[12]  M. Galinski,et al.  Plasmodium vivax: malarial proteins associated with the membrane-bound caveola-vesicle complexes and cytoplasmic cleft structures of infected erythrocytes. , 1990, Experimental parasitology.

[13]  I. Sherman.  Membrane structure and function of malaria parasites and the infected erythrocyte , 1985, Parasitology.

[14]  C. Whitty,et al.  A quantitative analysis of the microvascular sequestration of malaria parasites in the human brain. , 1999, The American journal of pathology.

[15]  N. White,et al.  Dynamic alteration in splenic function during acute falciparum malaria. , 1987, The New England journal of medicine.