OK/basigin expression on red blood cells varies between blood donors and correlates with binding of recombinant Plasmodium falciparum reticulocyte-binding protein homolog 5

Transfusion ◽  
2018 ◽  
Vol 58 (8) ◽  
pp. 2046-2053
Author(s):  
Luyi Ye ◽  
Fengyong Zhao ◽  
Qixiu Yang ◽  
Jiamin Zhang ◽  
Qin Li ◽  
...  
Keyword(s):  
Plasmodium Falciparum ◽  
Red Blood Cells ◽  
Blood Cells ◽  
Blood Donors ◽  
Binding Protein

scholarly journals Interactions between Plasmodium falciparum skeleton-binding protein 1 and the membrane skeleton of malaria-infected red blood cells

2015 ◽  
Vol 1848 (7) ◽  
pp. 1619-1628 ◽  
Author(s):  
Lev M. Kats ◽  
Nicholas I. Proellocks ◽  
Donna W. Buckingham ◽  
Lionel Blanc ◽  
John Hale ◽  
...  
Keyword(s):  
Plasmodium Falciparum ◽  
Red Blood Cells ◽  
Blood Cells ◽  
Binding Protein ◽  
Membrane Skeleton

Ultrastructural observations on the in vitro cytoadherence of Plasmodium falciparum infected red blood cells

1990 ◽  
Vol 48 (3) ◽  
pp. 914-915
Author(s):  
D.J.P. Ferguson ◽  
A.R. Berendt ◽  
J. Tansey ◽  
K. Marsh ◽  
C.I. Newbold
Keyword(s):  
Plasmodium Falciparum ◽  
Red Blood Cells ◽  
Blood Cells ◽  
Umbilical Vein ◽  
Cell Types ◽  
Amelanotic Melanoma ◽  
Cytoplasmic Process ◽  
Umbilical Vein Endothelial Cells

In human malaria, the most serious clinical manifestation is cerebral malaria (CM) due to infection with Plasmodium falciparum. The pathology of CM is thought to relate to the fact that red blood cells containing mature forms of the parasite (PRBC) cytoadhere or sequester to post capillary venules of various tissues including the brain. This in vivo phenomenon has been studied in vitro by examining the cytoadherence of PRBCs to various cell types and purified proteins. To date, three Ijiost receptor molecules have been identified; CD36, ICAM-1 and thrombospondin. The specific changes in the PRBC membrane which mediate cytoadherence are less well understood, but they include the sub-membranous deposition of electron-dense material resulting in surface deformations called knobs. Knobs were thought to be essential for cytoadherence, lput recent work has shown that certain knob-negative (K-) lines can cytoadhere. In the present study, we have used electron microscopy to re-examine the interactions between K+ PRBCs and both C32 amelanotic melanoma cells and human umbilical vein endothelial cells (HUVEC).We confirm previous data demonstrating that C32 cells possess numerous microvilli which adhere to the PRBC, mainly via the knobs (Fig. 1). In contrast, the HUVEC were relatively smooth and the PRBCs appeared partially flattened onto the cell surface (Fig. 2). Furthermore, many of the PRBCs exhibited an invagination of the limiting membrane in the attachment zone, often containing a cytoplasmic process from the endothelial cell (Fig. 2).

Endothelin-1 production by a microvascular endothelial cell line treated with Plasmodium falciparum parasitized red blood cells

2002 ◽  
Vol 103 (s2002) ◽  
pp. 464S-466S ◽  
Author(s):  
Nicoletta BASILICO ◽  
Livianna SPECIALE ◽  
Silvia PARAPINI ◽  
Pasquale FERRANTE ◽  
Donatella TARAMELLI
Keyword(s):  
Plasmodium Falciparum ◽  
Endothelial Cell ◽  
Red Blood Cells ◽  
Cell Line ◽  
Blood Cells ◽  
Microvascular Endothelial Cell ◽  
Microvascular Endothelium ◽  
Endothelial Cell Line ◽  
Endothelin 1 ◽  
Microvascular Endothelial

In this study, we investigated the production of endothelin 1 (ET-1) by a human microvascular endothelial cell line, HMEC-1, co-cultured with Plasmodium falciparum-parasitized red blood cells (pRBCs). The results indicate that hypoxia increased the basal level of ET-1 production by HMEC-1 cells after 24 or 48h of treatment. However, the co-incubation of HMEC-1 cells with pRBCs, but not with uninfected RBCs, induced a dose-dependent decrease of both constitutive and hypoxia-induced ET-1 production. The inhibition was not due to a decrease in cell viability, as lactate dehydrogenase release remained constant. These results indicate that pRBCs are able to interfere with both the constitutive and stimulated ET-1 release from the microvascular endothelium, thus inducing local modifications of the vascular tone and of the inflammatory response. This could be of relevance in the pathogenesis of the most severe forms of P. falciparum infections, such as cerebral malaria or malaria during pregnancy.

scholarly journals Dielectric characterization of Plasmodium falciparum -infected red blood cells using microfluidic impedance cytometry

2018 ◽  
Vol 15 (147) ◽  
pp. 20180416 ◽  
Author(s):  
C. Honrado ◽  
L. Ciuffreda ◽  
D. Spencer ◽  
L. Ranford-Cartwright ◽  
H. Morgan
Keyword(s):  
Plasmodium Falciparum ◽  
Dielectric Properties ◽  
Red Blood Cells ◽  
Blood Cells ◽  
Time Course ◽  
Fluorescent Protein ◽  
Clear Understanding ◽  
Infection Cycle ◽  
Dielectric Characterization ◽  
Impedance Cytometry

Although malaria is the world's most life-threatening parasitic disease, there is no clear understanding of how certain biophysical properties of infected cells change during the malaria infection cycle. In this article, we use microfluidic impedance cytometry to measure the dielectric properties of Plasmodium falciparum -infected red blood cells ( i- RBCs) at specific time points during the infection cycle. Individual parasites were identified within i- RBCs using green fluorescent protein (GFP) emission. The dielectric properties of cell sub-populations were determined using the multi-shell model. Analysis showed that the membrane capacitance and cytoplasmic conductivity of i- RBCs increased along the infection time course, due to membrane alterations caused by parasite infection. The volume ratio occupied by the parasite was estimated to vary from less than 10% at earlier stages, to approximately 90% at later stages. This knowledge could be used to develop new label-free cell sorting techniques for sample pre-enrichment, improving diagnosis.

scholarly journals Red blood cells release microparticles containing human argonaute 2 and miRNAs to target genes of Plasmodium falciparum

2017 ◽  
Vol 6 (1) ◽  
pp. 1-11 ◽  
Author(s):  
Zhensheng Wang ◽  
Juemin Xi ◽  
Xiao Hao ◽  
Weiwei Deng ◽  
Juan Liu ◽  
...  
Keyword(s):  
Plasmodium Falciparum ◽  
Red Blood Cells ◽  
Blood Cells ◽  
Target Genes ◽  
Argonaute 2

scholarly journals A Profound Membrane Reorganization Defines Susceptibility of Plasmodium falciparum Infected Red Blood Cells to Lysis by Granulysin and Perforin

2021 ◽  
Vol 12 ◽  
Author(s):  
Maria Andrea Hernández-Castañeda ◽  
Marilyne Lavergne ◽  
Pierina Casanova ◽  
Bryan Nydegger ◽  
Carla Merten ◽  
...  
Keyword(s):  
Plasmodium Falciparum ◽  
Red Blood Cells ◽  
Blood Cells ◽  
Molecular Mechanisms ◽  
Γδ T Cells ◽  
Parasite Growth ◽  
Complex Life Cycle ◽  
Cholesterol Depletion ◽  
Host Cell Membrane ◽  
Pore Forming Proteins

Malaria remains one of the most serious health problems in developing countries. The causative agent of malaria, Plasmodium spp., have a complex life cycle involving multiple developmental stages as well as different morphological, biochemical and metabolic requirements. We recently found that γδ T cells control parasite growth using pore-forming proteins to deliver their cytotoxic proteases, the granzymes, into blood residing parasites. Here, we follow up on the molecular mechanisms of parasite growth inhibition by human pore-forming proteins. We confirm that Plasmodium falciparum infection efficiently depletes the red blood cells of cholesterol, which renders the parasite surrounding membranes susceptible to lysis by prokaryotic membrane disrupting proteins, such as lymphocytic granulysin or the human cathelicidin LL-37. Interestingly, not the cholesterol depletion but rather the simultaneous exposure of phosphatidylserine, a negatively charged phospholipid, triggers resistance of late stage parasitized red blood cells towards the eukaryotic pore forming protein perforin. Overall, by revealing the molecular events we establish here a pathogen-host interaction that involves host cell membrane remodeling that defines the susceptibility towards cytolytic molecules.

scholarly journals Merocyanine 540-sensitized photoinactivation of human erythrocytes parasitized by Plasmodium falciparum

Blood ◽  
1992 ◽  
Vol 80 (1) ◽  
pp. 21-24 ◽  
Author(s):  
OM Smith ◽  
SA Dolan ◽  
JA Dvorak ◽  
TE Wellems ◽  
F Sieber
Keyword(s):  
Stem Cells ◽  
Plasmodium Falciparum ◽  
Hematopoietic Stem Cells ◽  
Red Blood Cells ◽  
Human Blood ◽  
Blood Cells ◽  
Potential Usefulness ◽  
Hematopoietic Stem ◽  
Infected Blood ◽  
Merocyanine 540

The purpose of this study was to evaluate the photosensitizing dye merocyanine 540 (MC540) as a means for extracorporeal purging of Plasmodium falciparum-infected erythrocytes from human blood. Parasitized red blood cells bound more dye than nonparasitized cells, and exposure to MC540 and light under conditions that are relatively well tolerated by normal erythrocytes and normal pluripotent hematopoietic stem cells reduced the concentration of parasitized cells by as much as 1,000-fold. Cells parasitized by the chloroquine- sensitive HB3 clone and the chloroquine-resistant Dd2 clone of P falciparum were equally susceptible to MC540-sensitized photolysis. These data suggest the potential usefulness of MC540 in the purging of P falciparum-infected blood.

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