Abnormal membrane phospholipid organization in <i>Plasmodium falciparum</i>‐infected human erythrocytes

Joshi, Prince; Gupta, C. M.

doi:10.1111/j.1365-2141.1988.tb06198.x

Cited by 37 publications

(16 citation statements)

References 22 publications

(11 reference statements)

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“…has been contradictory. For example, the results of Maguire et al [30] and Sherman, Prudhomme and Tait [31] agree with those of Joshi and Gupta [29,56] and Schwartz et al [57] in demonstrating PS exposure, but differ from the negative results of van der Schaft et al [58], Moll et al [59], and Taverne et al [60]. Indeed, Simoes et al [61] in commenting on these divergent findings suggested that it was excessive lysis, absence of glucose in the medium, and the use of buffers containing 100 mM KCl that resulted in "a dramatic change in phospholipid asymmetry".…”

Section: Discussionsupporting

confidence: 78%

Cytoadherence of Malaria-Infected Red Blood Cells Involves Exposure of Phosphatidylserine

Eda¹,

Sherman²

2002

Cell Physiol Biochem

146

122

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Phosphatidylserine (PS) is a membrane phospholipid which in intact cells is exclusively localized in the inner leaflet of the lipid bilayer. However, once cells undergo apoptosis or oxidative stress, PS molecules are exposed on the external surface of the cells and this contributes to their adherence to macrophages or endothelial cells. PS exposure on Plasmodium falciparum-infected red cells was determined by flow cytometry using fluorescein-labeled annexin V, which specifically binds to PS. Involvement of exposed PS in the adherence of malaria-infected red cells to endothelial cells was examined by in vitro cytoadherence assays. Infected cells exposed PS on their surface as the intracellular parasites matured to trophozoite and schizont stages. Adherence of malaria-infected cells to CD36, CD36-expressing Chinese hamster ovary cells, thrombospondin, and C32 amelanotic melanoma cells was inhibited by annexin V, whereas ICAM-1- and chondroitin sulfate A-mediated binding was not. Further, PS liposomes and glycerophosphorylserine, but not phosphatidylcholine liposomes and glycerophosphorylcholine, inhibited the binding of infected cells to CD36 and thrombospondin. In conclusion, these results demonstrate that PS exposed on the surface of malaria-infected red cells contributes, in part, to the adherence of P. falciparum-parasitized red cells to CD36 and thrombospondin.

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Section: Discussionsupporting

confidence: 78%

Cytoadherence of Malaria-Infected Red Blood Cells Involves Exposure of Phosphatidylserine

Eda¹,

Sherman²

2002

Cell Physiol Biochem

146

122

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“…Lipid asymmetry of the membrane, maintained by an aminophospholipid translocase activity, is reduced in aged erythrocytes 41 or erythrocytes under oxidative stress. 42 Altered membrane PL organization, particularly a greater PS exposure on the outer surface of the membrane, has been reported in both IRBCs 2,43,44 and URBCs, 45,46 although not confirmed by others. 29,47 Oxidative stress induced by P falciparum might contribute to the loss of PS by changing the transbilayer organization of the membrane phospholipids and enhancing PS exposure on the outer surface.…”

Section: Discussionmentioning

confidence: 87%

“…1,28 It is important to draw attention at this point to the paucity and conflicting nature of data reported in the literature when whole infected RBCs (reflecting the separate contribution of the erythrocyte and the intracellular parasite itself) are studied and when total RBC populations of infected and uninfected cells are compared with no prior fractionation. 1,2,5,29,30 This variability has been attributed to different parasite species, level of parasitemia, developmental stages of the parasite, or purity of cell membranes. On the basis of our results, additional factors, which can be controlled by standardizing the experimental methodology, contribute to these discrepancies.…”

Section: Discussionmentioning

confidence: 99%

Accelerated senescence of human erythrocytes cultured with Plasmodium falciparum

Omodeo‐Salè

Motti

Basilico

et al. 2003

Blood

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Red blood cells infected with Plasmodium falciparum (IRBCs) undergo changes primarily in their membrane composition that contribute to malaria pathogenesis. However, all manifestations (eg, anemia) cannot be accounted for by IRBCs alone. Uninfected erythrocytes (URBCs) may play a role, but they have been underresearched. We wanted to document changes in the erythrocyte membrane that could contribute to URBC reduced life span and malaria-associated anemia. Human erythrocytes were cultured with P falciparum and washed at the trophozoite stage. IRBCs and URBCs were separated on Percoll density gradient, thus obtaining erythrocyte fractions of different densities/ages. IRBC-and URBCpurified membranes were analyzed and compared with control normal erythrocytes (NRBCs) of the same age, from the same donor, kept in the same conditions. P falciparum accelerated aging of both IRBCs and URBCs, causing a significant shift in the cell population toward the denser (old) fraction. Protein, phospholipid, and cholesterol content were reduced in IRBCs and young URBCs. Young and medium uninfected fractions had higher levels of lipid peroxidation and phospholipid saturation (because of the loss of polyunsaturated fatty acids, PUFAs) and lower phosphatidylserine. In IRBCs, thiobarbituric reactive substances (TBARSs) were higher, and PUFAs and phosphatidylserine lower than in NRBCs and URBCs. In comparison, trophozoite membranes had lower phospholipid (particularly sphingomyelin and phosphatidylserine) and cholesterol content and a higher degree of saturation. Parasiteinduced peroxidative damage might account for these modifications. In summary, we demonstrated that membrane damage leading to accelerated senescence of both infected and uninfected erythrocytes will likely contribute to malaria anemia. (Blood. 2003;102:705-711)

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Section: Resultsmentioning

confidence: 99%

“…In addition, it has been previously reported (Browne & Hebbel, 1996) that thalassaemic patients' blood might contain RBC enriched with the adhesion molecule CD36 (which is absent in normal mature RBC). Both PS and CD36 can facilitate RBC/EC interaction, as elevated adhesion of RBC to EC observed in other RBC disorders, such as sickle cell anaemia and malaria, has been linked to elevated levels of PS (Joshi &Gupta, 1988) and CD36 (Wick &Eckman, 1996;McCormick et al, 1997).Of special interest in the present study is the different adherence of TM and TI RBC, but the clari®cation of this question is hindered by the mixture of pathological and normal RBC in the blood of TM patients who are routinely treated with blood transfusion. The studies of BorenstainBen-Yashar et al (1993) and Browne & Hebbel (1996), which investigated RBC of transfused TM patients, indicate that TI RBC might have a higher level of PS and CD36 than TM RBC.…”

mentioning

confidence: 99%

Enhanced adherence of β‐thalassaemic erythrocytes to endothelial cells

et al. 1999

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Summary. The adherence of red blood cells (RBC) to endothelial cells (EC), shown to correlate with microvascular occlusion in sickle cell disease and malaria, is considered a major contributor to microcirculatory disorders. In the present study the adherence to EC was markedly enhanced with RBC from b-thalassaemia major (TM) patients, and even more so with RBC from b-thalassaemia intermedia (TI) patients (10-fold and 25-fold higher than normal, respectively). It is proposed that enhanced RBC/EC adherence may contribute to the microcirculatory disorders observed in thalassaemia, especially in TI patients who are particularly known to suffer from leg ulcers.Keywords: b-thalassaemia major, b-thalassaemia intermedia, red blood cells, adhesion, endothelial cells.Blood¯ow is strongly in¯uenced by red blood cells (RBC)¯ow properties, namely RBC aggregability (their capacity to aggregate), deformability (ability to change shape) and adherence to endothelial cells (EC). These properties play a major role in haemodynamics, particularly in small blood vessels (the microcirculation), and their impairment has been linked to microcirculatory disorders in numerous pathological states.Thalassaemia (thal) is a congenital haemoglobinopathy, arising from imbalanced synthesis of either the alpha (a-thal) or the beta (b-thal) globin chain, which affects 1±2 million children annually throughout the world (Weatherall et al, 1995). Thalassaemia is characterized by morphological and functional erythrocyte anomalies, leading to chronic anaemia, severe iron overload in vital organs, and death in childhood or at adolescence. In addition, thalassaemic patients suffer from diverse clinical manifestations attributed to circulatory disorders, expressed by transient ischaemic attacks, microvessel obstruction leading to cerebral thrombosis and stroke, and chronic leg ulcers. b-thal patients are classi®ed as thal major (TM) or thal intermedia (TI) patients, mainly by the requirement for periodical blood transfusion in TM, which is not usually required for TI patients.The structural and functional abnormalities of thal RBC are associated with reduced deformability (Mohandas & Chasis, 1993) and increased aggregability (Chen et al, 1996). These are assumed to contribute to the microcirculatory disorders observed in thalassaemia.In recent years adhesion of RBC to EC has been considered to play an important role in the induction of vascular occlusion, as demonstrated in animal models of sickle cell disease and diabetes (Wautier et al, 1981;Kaul et al, 1993). In the present study we examined the adhesiveness of TM and TI RBC to EC, to further explore the possible role of RBC¯ow properties in thalassaemic microcirculatory disorders. METHODSBlood samples (2 ml) were received from volunteer TI and TM, splenectomized, patients. RBC were isolated by routine centrifugation, washed, and resuspended in culture medium (DMEM). The RBC were then placed on con¯uent cultured bovine aortic EC, in amounts suf®cient to cover the EC layer, and incubated for 45 min at 3...

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Abnormal membrane phospholipid organization in Plasmodium falciparum‐infected human erythrocytes

Cited by 37 publications

References 22 publications

Cytoadherence of Malaria-Infected Red Blood Cells Involves Exposure of Phosphatidylserine

Cytoadherence of Malaria-Infected Red Blood Cells Involves Exposure of Phosphatidylserine

Accelerated senescence of human erythrocytes cultured with Plasmodium falciparum

Enhanced adherence of β‐thalassaemic erythrocytes to endothelial cells

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