scholarly journals Differential Adhesive Properties of Sequestered Asexual and Sexual Stages of Plasmodium falciparum on Human Endothelial Cells Are Tissue Independent

PLoS ONE ◽  
2012 ◽  
Vol 7 (2) ◽  
pp. e31567 ◽  
Author(s):  
Francesco Silvestrini ◽  
Marta Tibúrcio ◽  
Lucia Bertuccini ◽  
Pietro Alano
Keyword(s):  
Endothelial Cells ◽  
Plasmodium Falciparum ◽  
Human Endothelial Cells ◽  
Adhesive Properties ◽  
Sexual Stages

scholarly journals Direct Activation of Human Endothelial Cells by Plasmodium falciparum-Infected Erythrocytes

2005 ◽  
Vol 73 (6) ◽  
pp. 3271-3277 ◽  
Author(s):  
Nicola K. Viebig ◽  
Ulrich Wulbrand ◽  
Reinhold Förster ◽  
Katherine T. Andrews ◽  
Michael Lanzer ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Plasmodium Falciparum ◽  
Endothelial Cell ◽  
Adhesion Molecule ◽  
Cell Activation ◽  
Physical Contact ◽  
Intercellular Adhesion Molecule ◽  
Immune Reactivity ◽  
Human Endothelial Cells ◽  
Tnf Α

ABSTRACT Cytoadherence of Plasmodium falciparum-infected erythrocytes (PRBC) to endothelial cells causes severe clinical disease, presumably as a of result perfusion failure and tissue hypoxia. Cytoadherence to endothelial cells is increased by endothelial cell activation, which is believed to occur in a paracrine fashion by mediators such as tumor necrosis factor alpha (TNF-α) released from macrophages that initially recognize PRBC. Here we provide evidence that PRBC directly stimulate human endothelial cells in the absence of macrophages, leading to increased expression of adhesion-promoting molecules, such as intercellular adhesion molecule 1. Endothelial cell stimulation by PRBC required direct physical contact for a short time (30 to 60 min) and was correlated with parasitemia. Gene expression profiling of endothelial cells stimulated by PRBC revealed increased expression levels of chemokine and adhesion molecule genes. PRBC-stimulated endothelial cells especially showed increased expression of molecules involved in parasite adhesion but failed to express molecules promoting leukocyte adhesion, such as E-selectin and vascular cell adhesion molecule 1, even after challenge with TNF-α. Collectively, our data suggest that stimulation of endothelial cells by PRBC may have two effects: prevention of parasite clearance through increased cytoadherence and attenuation of leukocyte binding to endothelial cells, thereby preventing deleterious immune reactivity.

Down-regulation of tight junction mRNAs in human endothelial cells co-cultured with Plasmodium falciparum-infected erythrocytes

2006 ◽  
Vol 55 (2) ◽  
pp. 107-112 ◽  
Author(s):  
Pannapa Susomboon ◽  
Yaowapa Maneerat ◽  
Paron Dekumyoy ◽  
Thareerat Kalambaheti ◽  
Moritoshi Iwagami ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Plasmodium Falciparum ◽  
Tight Junction ◽  
Human Endothelial Cells ◽  
Down Regulation

scholarly journals Inflammation Determines the Pro-Adhesive Properties of High Extracellular D-Glucose in Human Endothelial Cells In Vitro and Rat Microvessels In Vivo

PLoS ONE ◽  
2010 ◽  
Vol 5 (4) ◽  
pp. e10091 ◽  
Author(s):  
Verónica Azcutia ◽  
May Abu-Taha ◽  
Tania Romacho ◽  
Marta Vázquez-Bella ◽  
Nuria Matesanz ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Human Endothelial Cells ◽  
Adhesive Properties

Molecular Pathogenesis of Cerebral Malaria

1997 ◽  
Vol 3 (S2) ◽  
pp. 39-40
Author(s):  
H. Fujioka ◽  
M. Aikawa
Keyword(s):  
Endothelial Cells ◽  
Plasmodium Falciparum ◽  
Endothelial Cell ◽  
Cerebral Malaria ◽  
Infected Erythrocyte ◽  
Surface Proteins ◽  
Parasite Strain ◽  
Adhesive Properties ◽  
Rapid Changes ◽  
Cerebral Microvasculature

Plasmodium falciparum, the most malignant human malaria, is responsible for 2-3 million deaths annually. These infections often involve blockage of the cerebral microvasculature by P. falciparum-infected erythrocytes (Fig. 1). This aspect is considered the major factor in the pathogenesis of cerebral malaria.Upon invasion of the erythrocyte, P. falciparum immediately begins to remodel the infected erythrocyte. The adherence points of infected erythrocytes, termed knobs (Fig. 2 and 3), contain antigenically diverse 200-350kDa surface proteins (PfEMPl; Fig. 4). The PfEMPl variant surface proteins are encoded by a large and extremely diverse family of genes (var), and switches in the expression of var genes account for rapid changes in the antigenic and adhesive properties of P. falciparum-inkcted erythrocytes (2.4% per generation). Switches in the PfEMPl expression may not only affect the phenotype of the parasite strain but may also change its sequestration to endothelial cells. Genetic reorganization in this protein can lead to binding any of the following endothelial cell receptors; ICAM-1, CD36, thrombospondin, chondroitin sulfate (Fig. 5),2 ELAM-1, or VCAM-1.

Plasmodium falciparum: Effect of time in continuous culture on binding to human endothelial cells and amelanotic melanoma cells

1983 ◽  
Vol 56 (2) ◽  
pp. 207-214 ◽  
Author(s):  
Iroka J. Udeinya ◽  
Patricia M. Graves ◽  
Richard Carter ◽  
Masamichi Aikawa ◽  
Louis H. Miller
Keyword(s):  
Endothelial Cells ◽  
Plasmodium Falciparum ◽  
Continuous Culture ◽  
Melanoma Cells ◽  
Amelanotic Melanoma ◽  
Human Endothelial Cells

scholarly journals Erythrocyte stages of Plasmodium falciparum exhibit a high nitric oxide synthase (NOS) activity and release an NOS-inducing soluble factor.

1995 ◽  
Vol 182 (3) ◽  
pp. 677-688 ◽  
Author(s):  
D Ghigo ◽  
R Todde ◽  
H Ginsburg ◽  
C Costamagna ◽  
P Gautret ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Endothelial Cells ◽  
Plasmodium Falciparum ◽  
Red Blood Cells ◽  
Molecular Mass ◽  
Blood Cells ◽  
Soluble Factor ◽  
Human Endothelial Cells ◽  
Dose Dependent ◽  
Very High

Nitric oxide (NO), a highly diffusible cellular mediator involved in a wide range of biological effects, has been indicated as one of the cytotoxic agents released by leukocytes to counteract malaria infection. On the other hand, NO has been implicated as a mediator of the neuropathological symptoms of cerebral malaria. In such circumstances NO production has been thought to be induced in host tissues by host-derived cytokines. Here we provide evidence for the first time that human red blood cells infected by Plasmodium falciparum (IRBC) synthesize NO. The synthesis of NO (measured as citrulline and nitrate production) appeared to be very high in comparison with human endothelial cells; no citrulline and nitrate production was detectable in noninfected red blood cells. The NO synthase (NOS) activity was very high in the lysate of IRBC (while not measurable in that of normal red blood cells) and was inhibited in a dose-dependent way by three different NOS inhibitors (L-canavanine, NG-amino-L-arginine, and NG-nitro-L-arginine). NOS activity in P. falciparum IRBC is Ca++ independent, and the enzyme shows an apparent molecular mass < 100 kD, suggesting that the parasite expresses an isoform different from those found in mammalian cells. IRBC release a soluble factor able to induce NOS in human endothelial cells. Such NOS-inducing activity is not tissue specific, is time and dose dependent, requires de novo protein synthesis, and is probably associated with a thermolabile protein having a molecular mass > 100 kD. Our data suggest that an increased NO synthesis in P. falciparum malaria can be directly elicited by soluble factor(s) by the blood stages of the parasite, without necessarily requiring the intervention of host cytokines.

scholarly journals Plasmodium falciparum–Infected Erythrocyte Adhesion Induces Caspase Activation and Apoptosis in Human Endothelial Cells

2003 ◽  
Vol 187 (8) ◽  
pp. 1283-1290 ◽  
Author(s):  
Paco Pino ◽  
Ioannis Vouldoukis ◽  
Jean Pierre Kolb ◽  
Nassira Mahmoudi ◽  
Isabelle Desportes‐Livage ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Plasmodium Falciparum ◽  
Infected Erythrocyte ◽  
Caspase Activation ◽  
Human Endothelial Cells ◽  
Erythrocyte Adhesion
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