scholarly journals Invasion of mouse erythrocytes by the human malaria parasite, Plasmodium falciparum.

1987 ◽  
Vol 165 (6) ◽  
pp. 1713-1718 ◽  
Author(s):  
F W Klotz ◽  
J D Chulay ◽  
W Daniel ◽  
L H Miller
Keyword(s):  
Plasmodium Falciparum ◽  
Sialic Acid ◽  
Falciparum Malaria ◽  
Vaccine Development ◽  
Plasmodium Falciparum Malaria ◽  
Human Erythrocytes ◽  
Human Malaria Parasite ◽  
Parasite Plasmodium ◽  
Parasite Plasmodium Falciparum

Plasmodium falciparum malaria merozoites require erythrocyte sialic acid for optimal invasion of human erythrocytes. Since mouse erythrocytes have the form of sialic acid found on human erythrocytes (N-acetyl neuraminic acid), mouse erythrocytes were tested for invasion in vitro. The Camp and 7G8 strains of P. falciparum invaded mouse erythrocytes at 17-45% of the invasion rate of human erythrocytes. Newly invaded mouse erythrocytes morphologically resembled parasitized human erythrocytes as shown on Giemsa-stained blood films and by electron microscopy. The rim of parasitized mouse erythrocytes contained the P. falciparum 155-kD protein, which is on the rim of ring-infected human erythrocytes. Camp but not 7G8 invaded rat erythrocytes, indicating receptor heterogeneity. These data suggest that it may be possible to adapt the asexual erythrocytic stage of P. falciparum to rodents. The development of a rodent model of P. falciparum malaria could facilitate vaccine development.

scholarly journals Polymorphism of a high molecular weight schizont antigen of the human malaria parasite Plasmodium falciparum.

1985 ◽  
Vol 161 (1) ◽  
pp. 160-180 ◽  
Author(s):  
J S McBride ◽  
C I Newbold ◽  
R Anand
Keyword(s):  
Plasmodium Falciparum ◽  
Malaria Parasite ◽  
Peptide Mapping ◽  
Human Malaria Parasite ◽  
Human Malaria ◽  
Parasite Plasmodium ◽  
Parasite Plasmodium Falciparum ◽  
Immunological Classification ◽  
Specific Antigens

Intraspecies antigenic diversity in the blood stages of the human malaria parasite Plasmodium falciparum was investigated using a collection of murine monoclonal antibodies and clones of the parasite. The results were as follows: (a) The schizont and merozoite stages of the parasite express on their surface clonally restricted antigens detectable by strain-specific antibodies in indirect immunofluorescence tests. (b) These restricted antigens are phenotypically stable characteristics of clones grown in vitro. (c) The molecules carrying the specific antigens were isolated by immunoprecipitation and were found to be parasite proteins ranging in size from Mr 190,000 to 200,000 between clones. (d) Comparative immunoprecipitation and peptide mapping of these molecules showed that each parasite clone expresses a protein that is antigenically and structurally distinct from the equivalent products of several other clones. (e) The different clonal products are, however, immunologically interrelated, since they possess determinants in common with all tested isolates of the parasite. (f) These polymorphic molecules are closely related to a previously described schizont protein of P. falciparum that is posttranslationally cleaved into fragments located on the merozoite surface. These findings show the existence of a family of related polymorphic schizont antigens (PSA) of P. falciparum, whose expression is clonally restricted, and indicate that these proteins have regions of constant and variable antigenicity. We propose that a system of immunological classification of the parasite can be developed based on the polymorphism of these proteins.

scholarly journals The effect of purified aminoaldehydes produced by polyamine oxidation on the development in vitro of Plasmodium falciparum in normal and glucose-6-phosphate-dehydrogenase-deficient erythrocytes

1986 ◽  
Vol 236 (1) ◽  
pp. 97-101 ◽  
Author(s):  
D M L Morgan ◽  
U Bachrach ◽  
Y G Assaraf ◽  
E Harari ◽  
J Golenser
Keyword(s):  
Plasmodium Falciparum ◽  
Lethal Effect ◽  
Human Erythrocytes ◽  
Malarial Parasite ◽  
Parasite Plasmodium ◽  
Parasite Plasmodium Falciparum ◽  
Development In Vitro ◽  
Glucose 6 Phosphate Dehydrogenase ◽  
Polyamine Oxidation

Purified aminoaldehydes produced by polyamine oxidation were toxic to the malarial parasite, Plasmodium falciparum, cultured in human erythrocytes. There was a profound effect on young ring forms, and, during maturation, parasites became more sensitive to the aldehydes. Oxidation of the aldehydes abolished the lethal effect. The plasmodia within glucose-6-phosphate-dehydrogenase (G6PD)-deficient erythrocytes were more sensitive to mono- and di-aldehydes than were parasites in normal erythrocytes. G6PD-deficient erythrocytes were also more sensitive to pretreatment with the dialdehyde produced by the oxidation of spermine. Pretreatment prevented further invasion by the parasites.

Glutathione export from human erythrocytes and Plasmodium falciparum malaria parasites

2012 ◽  
Vol 448 (3) ◽  
pp. 389-400 ◽  
Author(s):  
Margery A. Barrand ◽  
Markus Winterberg ◽  
Frances Ng ◽  
Mai Nguyen ◽  
Kiaran Kirk ◽  
...  
Keyword(s):  
Plasmodium Falciparum ◽  
Plasmodium Falciparum Malaria ◽  
Human Erythrocytes ◽  
Multidrug Resistance Proteins ◽  
Resistance Proteins ◽  
Physiological Conditions ◽  
Parasite Plasmodium ◽  
Parasite Plasmodium Falciparum ◽  
Oxidative Challenge ◽  
New Permeability Pathways

Glutathione export from uninfected human erythrocytes was compared with that from cells infected with the malaria parasite Plasmodium falciparum using two separate methods that distinguish between oxidized (GSSG) and reduced (GSH) glutathione. One involved enzymatic recycling with or without thiol-masking; the other involved rapid derivatization followed by HPLC. Glutathione efflux from uninfected erythrocytes under physiological conditions occurred predominantly as GSH. On exposure of the cells to oxidative challenge, efflux of GSSG exceeded that of GSH. Efflux of both species was blocked by MK571, an inhibitor of mammalian multidrug-resistance proteins. Glutathione efflux from parasitized erythrocytes was substantially greater than that from uninfected erythrocytes. Under physiological conditions, the exported species was GSH, whereas under energy-depleted conditions, GSSG efflux occurred. Glutathione export from parasitized cells was inhibited partially by MK571 and more so by furosemide, an inhibitor of the ‘new permeability pathways’ induced by the parasite in the host erythrocyte membrane. Efflux from isolated parasites occurred as GSH. On exposure to oxidative challenge, this GSH efflux decreased, but no GSSG export was detected. These results are consistent with the view that the parasite supplies its host erythrocyte with GSH, much of which is exported from the infected cell via parasite-induced pathways.

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