Cytoadherence characteristics to endothelial receptors ICAM-1 and CD36 of<i>Plasmodium falciparum</i>populations from severe and uncomplicated malaria cases

Cojean, Sandrine; Jafari-Guemouri, Sayeh; Bras, J. Le; Durand, Rémy

doi:10.1051/parasite/2008152163

Cited by 15 publications

(10 citation statements)

References 29 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…iRBC sequestration at the microvascular site is an important feature of severe malaria. It has been shown that P. falciparum iRBC cytoadherence occurs via interactions of parasite surface antigen to endothelial receptor including ICAM-1 and CD36 [42], [43]. In this work we found an increase of ICAM-1 expression on renal tissue from P. berghei infected mice at day 7 post infection.…”

Section: Discussionsupporting

confidence: 55%

Oxidative Stress and Modification of Renal Vascular Permeability Are Associated with Acute Kidney Injury during P. berghei ANKA Infection

et al. 2012

View full text Add to dashboard Cite

Malaria associated-acute kidney injury (AKI) is associated with 45% of mortality in adult patients hospitalized with severe form of the disease. However, the causes that lead to a framework of malaria-associated AKI are still poorly characterized. Some clinical studies speculate that oxidative stress products, a characteristic of Plasmodium infection, as well as proinflammatory response induced by the parasite are involved in its pathophysiology. Therefore, we aimed to investigate the development of malaria-associated AKI during infection by P. berghei ANKA, with special attention to the role played by the inflammatory response and the involvement of oxidative stress. For that, we took advantage of an experimental model of severe malaria that showed significant changes in the renal pathophysiology to investigate the role of malaria infection in the renal microvascular permeability and tissue injury. Therefore, BALB/c mice were infected with P. berghei ANKA. To assess renal function, creatinine, blood urea nitrogen, and ratio of proteinuria and creatininuria were evaluated. The products of oxidative stress, as well as cytokine profile were quantified in plasma and renal tissue. The change of renal microvascular permeability, tissue hypoxia and cellular apoptosis were also evaluated. Parasite infection resulted in renal dysfunction. Furthermore, we observed increased expression of adhesion molecule, proinflammatory cytokines and products of oxidative stress, associated with a decrease mRNA expression of HO-1 in kidney tissue of infected mice. The measurement of lipoprotein oxidizability also showed a significant increase in plasma of infected animals. Together, our findings support the idea that products of oxidative stress, as well as the immune response against the parasite are crucial to changes in kidney architecture and microvascular endothelial permeability of BALB/c mice infected with P. berghei ANKA.

show abstract

Section: Discussionsupporting

confidence: 55%

Oxidative Stress and Modification of Renal Vascular Permeability Are Associated with Acute Kidney Injury during P. berghei ANKA Infection

et al. 2012

View full text Add to dashboard Cite

show abstract

“…P. falciparum isolates from children with UM have significantly higher levels of adhesion to CD36, under static conditions, than isolates from children with severe disease (CM, Severe Malaria-other and SMA). Previous studies had revealed that almost all isolates of P. falciparum adhere to CD36 [2], [42], [68], [69] and in Africa no differences in CD36-binding ability between SM and UM cases were observed [6], [25], [41], [70], although one study in Mali showed a positive association with a sub-type of PfEMP1 ( cys2var ) and severe malaria and this var type is part of a group of PfEMP1 proteins that tend to have lower binding to CD36 [71]. In adults in South East Asia, higher CD36 binding (using C32 cells) was observed among P. falciparum isolates from patients with severe (but not cerebral) malaria [72].…”

Section: Discussionmentioning

confidence: 99%

Specific Receptor Usage in Plasmodium falciparum Cytoadherence Is Associated with Disease Outcome

et al. 2011

View full text Add to dashboard Cite

Our understanding of the basis of severe disease in malaria is incomplete. It is clear that pathology is in part related to the pro-inflammatory nature of the host response but a number of other factors are also thought to be involved, including the interaction between infected erythrocytes and endothelium. This is a complex system involving several host receptors and a major parasite-derived variant antigen (PfEMP1) expressed on the surface of the infected erythrocyte membrane. Previous studies have suggested a role for ICAM-1 in the pathology of cerebral malaria, although these have been inconclusive. In this study we have examined the cytoadherence patterns of 101 patient isolates from varying clinical syndromes to CD36 and ICAM-1, and have used variant ICAM-1 proteins to further characterise this adhesive phenotype. Our results show that increased binding to CD36 is associated with uncomplicated malaria while ICAM-1 adhesion is raised in parasites from cerebral malaria cases.

show abstract

“…We were interested in hICAM-1, because it is one of the main adhesion molecules implicated in P. falciparum cytoadherence, particularly in the brain, and a target for new therapeutic approaches (Cojean et al, 2008;Turner et al, 1994;Wassmer et al, 2005). In the first case, hCMEC/D3 cells were transfected with a siRNA targeting hICAM-1 or an irrelevant siRNA (scramble (SCR) siRNA).…”

Section: Human Intercellular Adhesion Molecule 1 Is Involved In Parasmentioning

confidence: 99%

Metabolic Acidosis Induced by Plasmodium Falciparum Intraerythrocytic Stages Alters Blood—Brain Barrier Integrity

Zougbédé

Miller

Ravassard

et al. 2010

J Cereb Blood Flow Metab

View full text Add to dashboard Cite

The pathogenesis of cerebral malaria (CM) remains largely unknown. There is growing evidence that combination of both parasite and host factors could be involved in blood-brain barrier (BBB) breakdown. However, lack of adequate in vitro model of human BBB so far hampered molecular studies. In this article, we propose the use of hCMEC/D3 cells, a well-established human cerebral microvascular endothelial cell (EC) line, to study BBB breakdown induced by Plasmodium falciparum-parasitized red blood cells and environmental conditions. We show that coculture of parasitized erythrocytes with hCMEC/D3 cells induces cell adhesion and paracellular permeability increase, which correlates with disorganization of zonula occludens protein 1 expression pattern. Permeability increase and modification of tight junction proteins distribution are cytoadhesion independent. Finally, we show that permeability of hCMEC/D3 cell monolayers is mediated through parasite induced metabolic acidosis, which in turns correlates with apoptosis of parasitized erythrocytes. This new coculture model represents a very useful tool, which will improve the knowledge of BBB breakdown and the development of adjuvant therapies, together with antiparasitic drugs.

show abstract

Cytoadherence characteristics to endothelial receptors ICAM-1 and CD36 ofPlasmodium falciparumpopulations from severe and uncomplicated malaria cases

Cited by 15 publications

References 29 publications

Oxidative Stress and Modification of Renal Vascular Permeability Are Associated with Acute Kidney Injury during P. berghei ANKA Infection

Oxidative Stress and Modification of Renal Vascular Permeability Are Associated with Acute Kidney Injury during P. berghei ANKA Infection

Specific Receptor Usage in Plasmodium falciparum Cytoadherence Is Associated with Disease Outcome

Metabolic Acidosis Induced by Plasmodium Falciparum Intraerythrocytic Stages Alters Blood—Brain Barrier Integrity

Contact Info

Product

Resources

About