scholarly journals Thrombospondin mediates the cytoadherence of Plasmodium falciparum- infected red cells to vascular endothelium in shear flow conditions

Blood ◽  
1988 ◽  
Vol 71 (1) ◽  
pp. 71-75
Author(s):  
EP Rock ◽  
EF Jr Roth ◽  
RR Rojas-Corona ◽  
JA Sherwood ◽  
RL Nagel ◽  
...  
Keyword(s):  
Plasmodium Falciparum ◽  
Cerebral Malaria ◽  
Ex Vivo ◽  
Rabbit Antiserum ◽  
Immune Serum ◽  
Red Cells ◽  
Specific Attachment ◽  
Infected Cells ◽  
Human Immune ◽  
Venular Endothelium

Cerebral malaria is thought to involve specific attachment of Plasmodium falciparum-infected knobby red cells to venular endothelium. The nature of surface ligands on host endothelial cells that may mediate cytoadherence is poorly understood. We have investigated the effects of soluble thrombospondin, rabbit antiserum raised against thrombospondin, and human immune serum on cytoadherence of parasitized erythrocytes in ex vivo mesocecum vasculature. Preincubation of infected red cells with soluble thrombospondin or human immune serum inhibits binding of infected red cells to rat venular endothelium. Infusion of the microcirculatory preparation with rabbit antithrombospondin antibodies before perfusion of parasitized erythrocytes also resulted in decreased cytoadherence. In addition, incubation of infected cells with human immune sera obtained from malaria patients significantly inhibited the observed cytoadherence. Our results indicate that thrombospondin mediates binding of infected red cells to venular endothelium and may thus be involved in the pathogenesis of cerebral malaria.

scholarly journals Thrombospondin mediates the cytoadherence of Plasmodium falciparum- infected red cells to vascular endothelium in shear flow conditions

Blood ◽  
1988 ◽  
Vol 71 (1) ◽  
pp. 71-75 ◽  
Author(s):  
EP Rock ◽  
EF Jr Roth ◽  
RR Rojas-Corona ◽  
JA Sherwood ◽  
RL Nagel ◽  
...  
Keyword(s):  
Plasmodium Falciparum ◽  
Cerebral Malaria ◽  
Ex Vivo ◽  
Rabbit Antiserum ◽  
Immune Serum ◽  
Red Cells ◽  
Specific Attachment ◽  
Infected Cells ◽  
Human Immune ◽  
Venular Endothelium

Abstract Cerebral malaria is thought to involve specific attachment of Plasmodium falciparum-infected knobby red cells to venular endothelium. The nature of surface ligands on host endothelial cells that may mediate cytoadherence is poorly understood. We have investigated the effects of soluble thrombospondin, rabbit antiserum raised against thrombospondin, and human immune serum on cytoadherence of parasitized erythrocytes in ex vivo mesocecum vasculature. Preincubation of infected red cells with soluble thrombospondin or human immune serum inhibits binding of infected red cells to rat venular endothelium. Infusion of the microcirculatory preparation with rabbit antithrombospondin antibodies before perfusion of parasitized erythrocytes also resulted in decreased cytoadherence. In addition, incubation of infected cells with human immune sera obtained from malaria patients significantly inhibited the observed cytoadherence. Our results indicate that thrombospondin mediates binding of infected red cells to venular endothelium and may thus be involved in the pathogenesis of cerebral malaria.

scholarly journals An Opsonic Phagocytosis Assay for Plasmodium falciparum Sporozoites

2016 ◽  
Vol 24 (2) ◽  
Author(s):  
Ryan W. J. Steel ◽  
Brandon K. Sack ◽  
Moriya Tsuji ◽  
Mary Jane L. Navarro ◽  
Will Betz ◽  
...  
Keyword(s):  
Plasmodium Falciparum ◽  
Immune System ◽  
Immune Serum ◽  
Phagocytic Cells ◽  
Protein Targets ◽  
Content Type ◽  
Flow Cytometric ◽  
Blood Stage Infection ◽  
Human Immune

ABSTRACT Plasmodium falciparum malaria remains the deadliest parasitic disease worldwide. Vaccines targeting the preerythrocytic sporozoite and liver stages have the potential to entirely prevent blood-stage infection and disease, as well as onward transmission. Sporozoite surface and secreted proteins are leading candidates for inclusion in a preerythrocytic stage-specific, antibody-based vaccine. Preclinical functional assays to identify humoral correlates of protection in vitro and to validate novel sporozoite protein targets for inclusion in multisubunit vaccines currently do not consider the interaction of sporozoite-targeting antibodies with other components of the immune system. Here, we describe the development of a simple flow cytometric assay to quantitatively assess the ability of antibodies directed against P. falciparum sporozoites to facilitate their phagocytosis. We demonstrate that this sporozoite opsonic phagocytosis assay (SOPA) is compatible with both monoclonal antibodies and human immune serum and can be performed using cryopreserved P. falciparum sporozoites. This simple, accessible assay will aid with the assessment of antibody responses to vaccination with Plasmodium antigens and their interaction with phagocytic cells of the immune system.

Plasmodium falciparum: regional differences in lectin and cationized ferritin binding to the surface of the malaria-infected human erythrocyte

Parasitology ◽  
1986 ◽  
Vol 93 (1) ◽  
pp. 17-32 ◽  
Author(s):  
I. W. Sherman ◽  
Jane R. T. Greenan
Keyword(s):  
Electron Microscopy ◽  
Transmission Electron Microscopy ◽  
Plasmodium Falciparum ◽  
Uniform Distribution ◽  
Lectin Binding ◽  
Red Cells ◽  
Cationized Ferritin ◽  
Transmission Electron ◽  
Erythrocyte Surface ◽  
Infected Cells

SUMMARYThe distribution of anionic residues on the surface of erythrocytes infected withPlasmodium falciparumwas studied using cationized ferritin (CF) and transmission electron microscopy. CF staining of uninfected erythrocytes or erythrocytes infected with a knobless variant resulted in a dense and uniform distribution of ferritin particles; however, when red cells infected with a knob-inducing variant were exposed to CF, aggregates of ferritin particles were observed in the region of membrane elevation. Lectin binding to the erythrocyte surface was visualized by transmission electron microscopy using ferritin-conjugated lectins and lectin-fetuin-gold. No differences were observed in the lectin-binding patterns of malaria-infected or uninfected erythrocytes using WGA (wheat-germ agglutinin), RCA (ricin), andLimax flavuslectin. In distinct contrast to the uniform distribution of ferritin particles seen with these lectins was the appearance of clusters of ferritin-ConA over the knobby regions. Localized aggregates of ConA were not seen in knob-free areas or on the surface of red cells infected with a knobless variant. No significant differences were found in the agglutination reactions of normal and infected cells with theCancer antennariuslectin specific forO-acylated sialic acids.

scholarly journals Surface antigens of malaria merozoites. A high molecular weight precursor is processed to an 83,000 mol wt form expressed on the surface of Plasmodium falciparum merozoites.

1983 ◽  
Vol 158 (5) ◽  
pp. 1647-1653 ◽  
Author(s):  
R R Freeman ◽  
A A Holder
Keyword(s):  
Molecular Weight ◽  
Monoclonal Antibody ◽  
Plasmodium Falciparum ◽  
Surface Antigens ◽  
Immune Serum ◽  
Differential Centrifugation ◽  
Synchronous Cultures ◽  
Human Immune ◽  
High Yields ◽  
Major Surface

A technique was developed for obtaining high yields of naturally released Plasmodium falciparum merozoites from synchronous cultures of parasitized erythrocytes. The cultured erythrocytes were treated with trypsin to prevent reinvasion (6), and the released merozoites that accumulated extracellularly were harvested by differential centrifugation. The total biosynthetically labeled proteins of schizonts and merozoites, and those immunoprecipitated by human immune serum were analyzed and compared. The surface antigens of free merozoites, labeled by lactoperoxidase-catalyzed iodination, were also described. A monoclonal antibody, specific for a 195,000 mol wt schizont protein, and processing fragments derived from it (3) were used in immunoprecipitation and Western transfer analyses to determine which of the processing fragments are associated with merozoites and which of them are located on the merozoite surface. It was found that processing of the 195,000 mol wt precursor down to an 83,000 mol wt fragment is complete in free merozoites, and that this fragment is expressed as one of the major surface antigens of P. falciparum merozoites.

Induction of crisis forms in cultured Plasmodium falciparum with human immune serum from Sudan

Science ◽  
1982 ◽  
Vol 216 (4551) ◽  
pp. 1230-1233 ◽  
Author(s):  
J. Jensen ◽  
M. Boland ◽  
M Akood
Keyword(s):  
Plasmodium Falciparum ◽  
Immune Serum ◽  
Human Immune

Increased rigidity of red cells in patients with Plasmodium falciparum, and its possible relation to cerebral malaria

1995 ◽  
Vol 15 (5) ◽  
pp. 729-735
Author(s):  
Petcharindr Yamarat ◽  
Yupa Chantachum ◽  
Napachai Suthisai ◽  
Bangon Sukchut
Keyword(s):  
Plasmodium Falciparum ◽  
Cerebral Malaria ◽  
Red Cells

Differential Outcomes for Long Term ex vivo Lung Perfusion in a Porcine Model - With or without Red Cells?

2015 ◽  
Vol 63 (S 01) ◽  
Author(s):  
W. Sommer ◽  
M. Avsar ◽  
J. Salman ◽  
C. Kühn ◽  
I. Tudorache ◽  
...  
Keyword(s):  
Porcine Model ◽  
Ex Vivo ◽  
Lung Perfusion ◽  
Red Cells ◽  
Ex Vivo Lung Perfusion ◽  
Differential Outcomes

IN VITRO DESTRUCTION OF LEISHMANIA DONOVANI INFECTED CELLS BY IMMUNE SERUM

1976 ◽  
Vol 4 (3-4) ◽  
pp. 207-211
Author(s):  
SHUN SHINBO ◽  
TAKATOSHI KOBAYAKAWA ◽  
HIROSHI ISHIYAMA ◽  
KAZUSHIGE MASUDA
Keyword(s):  
Leishmania Donovani ◽  
Immune Serum ◽  
Infected Cells

scholarly journals Malaria parasites both repress host CXCL10 and use it as a cue for growth acceleration

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Yifat Ofir-Birin ◽  
Hila Ben Ami Pilo ◽  
Abel Cruz Camacho ◽  
Ariel Rudik ◽  
Anna Rivkin ◽  
...  
Keyword(s):  
Plasmodium Falciparum ◽  
Life Cycle ◽  
Cerebral Malaria ◽  
Survival Strategy ◽  
Parasitic Disease ◽  
Malaria Parasites ◽  
Sensing System ◽  
Rich Domain ◽  
Cargo Delivery ◽  
Low Levels

AbstractPathogens are thought to use host molecular cues to control when to initiate life-cycle transitions, but these signals are mostly unknown, particularly for the parasitic disease malaria caused by Plasmodium falciparum. The chemokine CXCL10 is present at high levels in fatal cases of cerebral malaria patients, but is reduced in patients who survive and do not have complications. Here we show a Pf ‘decision-sensing-system’ controlled by CXCL10 concentration. High CXCL10 expression prompts P. falciparum to initiate a survival strategy via growth acceleration. Remarkably, P. falciparum inhibits CXCL10 synthesis in monocytes by disrupting the association of host ribosomes with CXCL10 transcripts. The underlying inhibition cascade involves RNA cargo delivery into monocytes that triggers RIG-I, which leads to HUR1 binding to an AU-rich domain of the CXCL10 3’UTR. These data indicate that when the parasite can no longer keep CXCL10 at low levels, it can exploit the chemokine as a cue to shift tactics and escape.

Sign in / Sign up

Export Citation Format

Share Document