Rolling and stationary cytoadhesion of red blood cells parasitized by <i>Plasmodium falciparum</i>: separate roles for ICAM‐1, CD36 and thrombospondin

Cooke, Brian M.; Berendt, Anthony R.; Craig, Alister G.; MacGregor, John S.; Newbold, C I; Nash, Gerard B.

doi:10.1111/j.1365-2141.1994.tb04887.x

Cited by 179 publications

(155 citation statements)

References 27 publications

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“…Furthermore, it has been proposed that group A PfEMP1 proteins are not under selection for ICAM-1-binding DBLb domains (22), and large group B and group C PfEMP1 proteins appear to be under selection for concomitant adhesion to ICAM-1 and CD36 (24,44). Because IE adhesion to CD36 is associated with uncomplicated malaria (21), these observations can be seen as arguments against an important role for ICAM-1-specific IE adhesion in the pathogenesis of severe P. falciparum malaria, not least CM.…”

Section: Discussionmentioning

confidence: 99%

A Novel Domain Cassette Identifies Plasmodium falciparum PfEMP1 Proteins Binding ICAM-1 and Is a Target of Cross-Reactive, Adhesion-Inhibitory Antibodies

Bengtsson

Joergensen

Rask

et al. 2013

The Journal of Immunology

106

175

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Cerebral Plasmodium falciparum malaria is characterized by adhesion of infected erythrocytes (IEs) to the cerebral microvasculature. This has been linked to parasites expressing the structurally related group A subset of the P. falciparum erythrocyte membrane protein 1 (PfEMP1) family of IE adhesion ligands and to IEs with affinity for ICAM-1. However, recent evidence has cast doubt on both these associations, tempering hopes of the feasibility of developing a vaccine based on ICAM-1–binding PfEMP1. In this study, we report the identification of a domain cassette (DC) present in group A var genes from six genetically distinct P. falciparum parasites. The three domains in the cassette, which we call DC4, had a high level of sequence identity and cluster together phylogenetically. Erythrocytes infected by these parasites and selected in vitro for expression of DC4 adhered specifically to ICAM-1. The ICAM-1–binding capacity of DC4 was mapped to the C-terminal third of its Duffy-binding–like β3 domain. DC4 was the target of broadly cross-reactive and adhesion-inhibitory IgG Abs, and levels of DC4-specific and adhesion-inhibitory IgG increased with age among P. falciparum–exposed children. Our study challenges earlier conclusions that group A PfEMP1 proteins are not central to ICAM-1–specific IE adhesion and support the feasibility of developing a vaccine preventing cerebral malaria by inhibiting cerebral IE sequestration.

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Section: Discussionmentioning

confidence: 99%

A Novel Domain Cassette Identifies Plasmodium falciparum PfEMP1 Proteins Binding ICAM-1 and Is a Target of Cross-Reactive, Adhesion-Inhibitory Antibodies

Bengtsson

Joergensen

Rask

et al. 2013

The Journal of Immunology

106

175

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“…This adherence of Pf-RBCs is believed to be the main cause of bleeding complications in cerebral malaria due to blockages of small vessels in the brain (7). Unlike the extensive research on leukocytes, very few in vitro experiments (8)(9)(10)(11) have examined the adhesive dynamics of Pf-RBCs. For example, in ref.…”

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confidence: 99%

Quantifying the biophysical characteristics of Plasmodium-falciparum -parasitized red blood cells in microcirculation

Fedosov

Caswell

Suresh

et al. 2010

Proc. Natl. Acad. Sci. U.S.A.

169

141

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The pathogenicity of Plasmodium falciparum (Pf) malaria results from the stiffening of red blood cells (RBCs) and its ability to adhere to endothelial cells (cytoadherence). The dynamics of Pf-parasitized RBCs is studied by three-dimensional mesoscopic simulations of flow in cylindrical capillaries in order to predict the flow resistance enhancement at different parasitemia levels. In addition, the adhesive dynamics of Pf-RBCs is explored for various parameters revealing several types of cell dynamics such as firm adhesion, very slow slipping along the wall, and intermittent flipping. The parasite inside the RBC is modeled explicitly in order to capture phenomena such as "hindered tumbling" motion of the RBC and the sudden transition from firm RBC cytoadherence to flipping on the endothelial surface. These predictions are in quantitative agreement with recent experimental observations, and thus the three-dimensional modeling method presented here provides new capabilities for guiding and interpreting future in vitro and in vivo studies of malaria.adhesion | erythrocyte | malaria | mechanical properties | dissipative particle dynamics R ed blood cells parasitized by Plasmodium falciparum (Pf-RBCs) undergo irreversible changes in structure and biophysical characteristics, which can lead to drastically altered blood circulation. The membrane shear modulus of infected RBCs may increase up to ten-fold causing capillary occlusions (1, 2), thereby resulting in substantial increase in resistance to blood flow. Such effects may be intensified due to the enhanced cytoadherence of Pf-RBCs to the vascular endothelium (3-6). This adherence of Pf-RBCs is believed to be the main cause of bleeding complications in cerebral malaria due to blockages of small vessels in the brain (7). Unlike the extensive research on leukocytes, very few in vitro experiments (8-11) Recent progress in multiscale numerical modeling (12-14) allows us to model soft matter, and RBCs in particular, at sufficient detail, i.e., simulating nanometer scales while simultaneously capturing the large scale dynamics. We have developed and validated a Dissipative Particle Dynamics (DPD) model (12, 14-16) that can accurately simulate the properties and dynamic behavior of healthy RBCs as well as Pf-RBCs. The multiscale model can represent a RBC at the spectrin level with 30,000 points (17) or at a coarser level with 500 points by proper scaling of the physiologically correct parameters (12, 14, 15); hence, no ad hoc calibration is required. The predictive capability of the DPD model has been demonstrated in comparisons with microfluidic experiments that probe controlled pressure-velocity relationships of (healthy) RBC flow through microchannels whose inner openings mimic the smallest dimensions for RBC passage in the microvasculature (16). In addition, we have extended the adhesive dynamics model of (18,19) to the DPD framework, and validated it by simulating the adhesive dynamics of leukocytes for which extensive experimental results exist (20,21). In summary, ...

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“…For Plasmodium falciparum, it is well known that molecules such as ICAM-1, PECAM-1, E-selectin and VCAM-1 act as receptors of ligands on the parasitized red blood cells (Cooke et al 1994, Chen et al 2000, Senezuk et al 2001. These findings suggest that some of these molecules could act as receptors for the adhesion of red blood cells to the vascular endothelium in animals infected by B. bovis.…”

Section: Discussionmentioning

confidence: 76%

Babesia bovis: expression of adhesion molecules in bovine umbilical endothelial cells stimulated with plasma from infected cattle

et al. 2014

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Pesq. Vet. Bras. 34(10):937-941, outubro 2014 937 RESUMO.-[Babesia bovis: expressão de moléculas de adesão em células endoteliais de cordão umbilical de bovinos estimuladas com plasma de bovinos infectados.] Dez bezerros machos, da raça Jersey, com 1 ano de idade com baços "in situ", sorológica e parasitologicamente livres de Babesia, foram mantidos em baias individuais no isolamento a prova de artrópodes do Depto de Veterinária desde o nascimento e ao longo de toda a experimentação. Os animais foram divididos aleatoriamente em dois grupos. Cinco animais (grupo A) foram inoculados por via intravenosa com 6,6 x10 7 hemácias parasitados com amostra patogênica de Babesia bovis (BboUFV -1 7 ª passagem) , para a determinação subseqüente "ex vivo" da expressão de moléculas de adesão . Cinco animais não inoculados (Grupo B ) foram utilizados como controlo negativo . A expressão de moléculas de adesão ICAM -1, VCAM , PECAM -1, E -selectina e trombospondina ( TSP ) foi medida em células endoteliais da veia umbilical de bovinos (BUVECs). As células endoteliais estimuladas com um pool de plasma proveniente de animais infectados com BboUFV -1 7 ª passagem tinham uma imunocoloração muito mais intensa de ICAM -1 , VCAM , PECAM -1 de E -selectina e de TSP , em comparação com as células que não receberam o estímulo . Os resultados sugerem que as citocinas pró-inflamatórias liberados na fase aguda da babesiose pode estar envolvida na expressão de moléculas de adesão , implicando , assim, elas na fisiopatologia da babesiose causada por B. bovis. Ten male, 12-month-old Jersey with intact spleens, serologically and parasitologically free from Babesia were housed individually in an arthropod-free isolation system from birth and throughout entire experiment. The animals were randomly divided into two groups. Five animals (group A) were intravenously inoculated with 6.6 X10 7 red blood cells parasitized with pathogenic sample of Babesia bovis (passage 7 BboUFV-1), for the subsequent "ex vivo" determination of the expression of adhesion molecules. Five non-inoculated animals (group B) were used as the negative control. The expression of the adhesion molecules ICAM-1, VCAM, PECAM-1 E-selectin and thrombospondin (TSP) was measured in bovine umbilical vein endothelial cells (BUVECs). The endothelial cells stimulated with a pool of plasma from animals infected with the BboUFV-1 7 th passage sample had a much more intense immunostaining of ICAM-1, VCAM, PECAM-1 E-selectin and TSP, compared to the cells which did not received the stimulus. The results suggest that proinflammatory cytokines released in the acute phase of babesiosis may be involved in the expression of adhesion molecules thereby implicating them in the pathophysiology of babesiosis caused by B. bovis.

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Rolling and stationary cytoadhesion of red blood cells parasitized by Plasmodium falciparum: separate roles for ICAM‐1, CD36 and thrombospondin

Cited by 179 publications

References 27 publications

A Novel Domain Cassette Identifies Plasmodium falciparum PfEMP1 Proteins Binding ICAM-1 and Is a Target of Cross-Reactive, Adhesion-Inhibitory Antibodies

A Novel Domain Cassette Identifies Plasmodium falciparum PfEMP1 Proteins Binding ICAM-1 and Is a Target of Cross-Reactive, Adhesion-Inhibitory Antibodies

Quantifying the biophysical characteristics of Plasmodium-falciparum -parasitized red blood cells in microcirculation

Babesia bovis: expression of adhesion molecules in bovine umbilical endothelial cells stimulated with plasma from infected cattle

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