The Microcirculation in Severe Malaria
Identifieur interne : 00A870 ( Main/Exploration ); précédent : 00A869; suivant : 00A871The Microcirculation in Severe Malaria
Auteurs : Stephen J. Rogerson [Australie] ; Georges E. Grau [France] ; Nicholas H. Hunt [Australie]Source :
- Microcirculation [ 1073-9688 ] ; 2004-10-11.
Descripteurs français
- Wicri :
- topic : Médiateur.
English descriptors
- KwdEn :
- Acad, Adhesion, African children, Aikawa, Berendt, Birth weight, Blood cells, Brain microvessels, Cerebral, Cerebral endothelium, Cerebral malaria, Cerebral vessels, Cerebrospinal fluid, Chondroitin, Chondroitin sulfate, Clinical disease, Coma, Cytoadherence, Cytoadherence characteristics, Cytokine, Dendritic cells, Disease severity, Endothelial, Endothelial cells, Endothelial receptors, Endothelium, Erythrocyte, Experimental murine, Falciparum, Falciparum malaria, Fatal murine, Fibrin deposition, Flow conditions, Grau, Greenwood, Host receptors, Human microvascular, Human placenta, Human studies, Immune, Immunol, Inflammatory, Intercellular, Intercellular adhesion, Intervillous, Intervillous space, Kynurenine pathway, Lancet, Leukocyte, Looareesuwan, Malaria, Malaria infection, Malaria pathogenesis, Malaria pigment, Malarial, Medana, Mediator, Microcirculation, Microvascular, Microvessels, Model systems, Molyneux, Monocyte, Murine, Neuronal damage, Newbold, Nitric, Nitric oxide, Noncerebral malaria, Other receptors, Parasite, Parasitized, Parasitized erythrocytes, Parasitol, Parasitol today, Pathogenesis, Pathol, Pathway, Pfemp1, Placenta, Placental, Placental malaria, Plasmodium, Plasmodium erythrocytes, Plasmodium falciparum, Plasmodium falciparum cytoadherence, Plasmodium falciparum erythrocyte membrane protein, Platelet, Platelet accumulation, Pregnant women, Proc natl acad, Quinolinic acid, Receptor, Reeder, Rogerson, Rosette, Rosetting, Sequestration, Severe falciparum malaria, Severe malaria, Stocker, Sulfate, Trans, Tryptophan metabolism, Tumor necrosis factor, Uninfected erythrocytes, Vascular cell adhesion molecule, Wahlgren.
- Teeft :
- Acad, Adhesion, African children, Aikawa, Berendt, Birth weight, Blood cells, Brain microvessels, Cerebral, Cerebral endothelium, Cerebral malaria, Cerebral vessels, Cerebrospinal fluid, Chondroitin, Chondroitin sulfate, Clinical disease, Coma, Cytoadherence, Cytoadherence characteristics, Cytokine, Dendritic cells, Disease severity, Endothelial, Endothelial cells, Endothelial receptors, Endothelium, Erythrocyte, Experimental murine, Falciparum, Falciparum malaria, Fatal murine, Fibrin deposition, Flow conditions, Grau, Greenwood, Host receptors, Human microvascular, Human placenta, Human studies, Immune, Immunol, Inflammatory, Intercellular, Intercellular adhesion, Intervillous, Intervillous space, Kynurenine pathway, Lancet, Leukocyte, Looareesuwan, Malaria, Malaria infection, Malaria pathogenesis, Malaria pigment, Malarial, Medana, Mediator, Microcirculation, Microvascular, Microvessels, Model systems, Molyneux, Monocyte, Murine, Neuronal damage, Newbold, Nitric, Nitric oxide, Noncerebral malaria, Other receptors, Parasite, Parasitized, Parasitized erythrocytes, Parasitol, Parasitol today, Pathogenesis, Pathol, Pathway, Pfemp1, Placenta, Placental, Placental malaria, Plasmodium, Plasmodium erythrocytes, Plasmodium falciparum, Plasmodium falciparum cytoadherence, Plasmodium falciparum erythrocyte membrane protein, Platelet, Platelet accumulation, Pregnant women, Proc natl acad, Quinolinic acid, Receptor, Reeder, Rogerson, Rosette, Rosetting, Sequestration, Severe falciparum malaria, Severe malaria, Stocker, Sulfate, Trans, Tryptophan metabolism, Tumor necrosis factor, Uninfected erythrocytes, Vascular cell adhesion molecule, Wahlgren.
Abstract
Severe malaria in humans and animals is initiated by interactions between malaria‐infected cells, host blood cells (including monocytes, T cells and platelets) and endothelial cells of the microcirculation. Adhesion to vascular cells, and possible vascular obstruction in severe human disease, involves interaction between host receptors and parasite‐derived proteins, such as the variant antigen Plasmodium falciparum erythrocyte membrane protein 1 (PfEMP1). Our understanding of how different PfEMP1 variants may target infected erythrocytes to specific sites, such as the placenta, is rapidly increasing. However, in most instances downstream immune‐mediated inflammatory processes appear more central than parasite accumulation to development of severe malaria. Using genetically‐manipulated animal models of severe malaria, key roles for CD8 T cells and mediators such as lymphotoxin in the pathogenesis of murine disease have been established. Experimental and human studies suggest vascular deposition of activated platelets may have a central role. Here, we review some recent advances in the understanding of severe malaria pathogenesis from human and animal studies, focusing on events at the level of the microcirculation, and highlight the role for activated host cells in initiating the pathology of the disease.
Url:
DOI: 10.1080/10739680490503311
Affiliations:
- Australie, France
- Nouvelle-Galles du Sud, Provence-Alpes-Côte d'Azur, Victoria (État)
- Marseille, Melbourne, Sydney
- Université de Melbourne, Université de Sydney, Université de la Méditerranée
Links toward previous steps (curation, corpus...)
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Le document en format XML
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<term>Adhesion</term>
<term>African children</term>
<term>Aikawa</term>
<term>Berendt</term>
<term>Birth weight</term>
<term>Blood cells</term>
<term>Brain microvessels</term>
<term>Cerebral</term>
<term>Cerebral endothelium</term>
<term>Cerebral malaria</term>
<term>Cerebral vessels</term>
<term>Cerebrospinal fluid</term>
<term>Chondroitin</term>
<term>Chondroitin sulfate</term>
<term>Clinical disease</term>
<term>Coma</term>
<term>Cytoadherence</term>
<term>Cytoadherence characteristics</term>
<term>Cytokine</term>
<term>Dendritic cells</term>
<term>Disease severity</term>
<term>Endothelial</term>
<term>Endothelial cells</term>
<term>Endothelial receptors</term>
<term>Endothelium</term>
<term>Erythrocyte</term>
<term>Experimental murine</term>
<term>Falciparum</term>
<term>Falciparum malaria</term>
<term>Fatal murine</term>
<term>Fibrin deposition</term>
<term>Flow conditions</term>
<term>Grau</term>
<term>Greenwood</term>
<term>Host receptors</term>
<term>Human microvascular</term>
<term>Human placenta</term>
<term>Human studies</term>
<term>Immune</term>
<term>Immunol</term>
<term>Inflammatory</term>
<term>Intercellular</term>
<term>Intercellular adhesion</term>
<term>Intervillous</term>
<term>Intervillous space</term>
<term>Kynurenine pathway</term>
<term>Lancet</term>
<term>Leukocyte</term>
<term>Looareesuwan</term>
<term>Malaria</term>
<term>Malaria infection</term>
<term>Malaria pathogenesis</term>
<term>Malaria pigment</term>
<term>Malarial</term>
<term>Medana</term>
<term>Mediator</term>
<term>Microcirculation</term>
<term>Microvascular</term>
<term>Microvessels</term>
<term>Model systems</term>
<term>Molyneux</term>
<term>Monocyte</term>
<term>Murine</term>
<term>Neuronal damage</term>
<term>Newbold</term>
<term>Nitric</term>
<term>Nitric oxide</term>
<term>Noncerebral malaria</term>
<term>Other receptors</term>
<term>Parasite</term>
<term>Parasitized</term>
<term>Parasitized erythrocytes</term>
<term>Parasitol</term>
<term>Parasitol today</term>
<term>Pathogenesis</term>
<term>Pathol</term>
<term>Pathway</term>
<term>Pfemp1</term>
<term>Placenta</term>
<term>Placental</term>
<term>Placental malaria</term>
<term>Plasmodium</term>
<term>Plasmodium erythrocytes</term>
<term>Plasmodium falciparum</term>
<term>Plasmodium falciparum cytoadherence</term>
<term>Plasmodium falciparum erythrocyte membrane protein</term>
<term>Platelet</term>
<term>Platelet accumulation</term>
<term>Pregnant women</term>
<term>Proc natl acad</term>
<term>Quinolinic acid</term>
<term>Receptor</term>
<term>Reeder</term>
<term>Rogerson</term>
<term>Rosette</term>
<term>Rosetting</term>
<term>Sequestration</term>
<term>Severe falciparum malaria</term>
<term>Severe malaria</term>
<term>Stocker</term>
<term>Sulfate</term>
<term>Trans</term>
<term>Tryptophan metabolism</term>
<term>Tumor necrosis factor</term>
<term>Uninfected erythrocytes</term>
<term>Vascular cell adhesion molecule</term>
<term>Wahlgren</term>
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<keywords scheme="Teeft" xml:lang="en"><term>Acad</term>
<term>Adhesion</term>
<term>African children</term>
<term>Aikawa</term>
<term>Berendt</term>
<term>Birth weight</term>
<term>Blood cells</term>
<term>Brain microvessels</term>
<term>Cerebral</term>
<term>Cerebral endothelium</term>
<term>Cerebral malaria</term>
<term>Cerebral vessels</term>
<term>Cerebrospinal fluid</term>
<term>Chondroitin</term>
<term>Chondroitin sulfate</term>
<term>Clinical disease</term>
<term>Coma</term>
<term>Cytoadherence</term>
<term>Cytoadherence characteristics</term>
<term>Cytokine</term>
<term>Dendritic cells</term>
<term>Disease severity</term>
<term>Endothelial</term>
<term>Endothelial cells</term>
<term>Endothelial receptors</term>
<term>Endothelium</term>
<term>Erythrocyte</term>
<term>Experimental murine</term>
<term>Falciparum</term>
<term>Falciparum malaria</term>
<term>Fatal murine</term>
<term>Fibrin deposition</term>
<term>Flow conditions</term>
<term>Grau</term>
<term>Greenwood</term>
<term>Host receptors</term>
<term>Human microvascular</term>
<term>Human placenta</term>
<term>Human studies</term>
<term>Immune</term>
<term>Immunol</term>
<term>Inflammatory</term>
<term>Intercellular</term>
<term>Intercellular adhesion</term>
<term>Intervillous</term>
<term>Intervillous space</term>
<term>Kynurenine pathway</term>
<term>Lancet</term>
<term>Leukocyte</term>
<term>Looareesuwan</term>
<term>Malaria</term>
<term>Malaria infection</term>
<term>Malaria pathogenesis</term>
<term>Malaria pigment</term>
<term>Malarial</term>
<term>Medana</term>
<term>Mediator</term>
<term>Microcirculation</term>
<term>Microvascular</term>
<term>Microvessels</term>
<term>Model systems</term>
<term>Molyneux</term>
<term>Monocyte</term>
<term>Murine</term>
<term>Neuronal damage</term>
<term>Newbold</term>
<term>Nitric</term>
<term>Nitric oxide</term>
<term>Noncerebral malaria</term>
<term>Other receptors</term>
<term>Parasite</term>
<term>Parasitized</term>
<term>Parasitized erythrocytes</term>
<term>Parasitol</term>
<term>Parasitol today</term>
<term>Pathogenesis</term>
<term>Pathol</term>
<term>Pathway</term>
<term>Pfemp1</term>
<term>Placenta</term>
<term>Placental</term>
<term>Placental malaria</term>
<term>Plasmodium</term>
<term>Plasmodium erythrocytes</term>
<term>Plasmodium falciparum</term>
<term>Plasmodium falciparum cytoadherence</term>
<term>Plasmodium falciparum erythrocyte membrane protein</term>
<term>Platelet</term>
<term>Platelet accumulation</term>
<term>Pregnant women</term>
<term>Proc natl acad</term>
<term>Quinolinic acid</term>
<term>Receptor</term>
<term>Reeder</term>
<term>Rogerson</term>
<term>Rosette</term>
<term>Rosetting</term>
<term>Sequestration</term>
<term>Severe falciparum malaria</term>
<term>Severe malaria</term>
<term>Stocker</term>
<term>Sulfate</term>
<term>Trans</term>
<term>Tryptophan metabolism</term>
<term>Tumor necrosis factor</term>
<term>Uninfected erythrocytes</term>
<term>Vascular cell adhesion molecule</term>
<term>Wahlgren</term>
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<keywords scheme="Wicri" type="topic" xml:lang="fr"><term>Médiateur</term>
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<front><div type="abstract" xml:lang="en">Severe malaria in humans and animals is initiated by interactions between malaria‐infected cells, host blood cells (including monocytes, T cells and platelets) and endothelial cells of the microcirculation. Adhesion to vascular cells, and possible vascular obstruction in severe human disease, involves interaction between host receptors and parasite‐derived proteins, such as the variant antigen Plasmodium falciparum erythrocyte membrane protein 1 (PfEMP1). Our understanding of how different PfEMP1 variants may target infected erythrocytes to specific sites, such as the placenta, is rapidly increasing. However, in most instances downstream immune‐mediated inflammatory processes appear more central than parasite accumulation to development of severe malaria. Using genetically‐manipulated animal models of severe malaria, key roles for CD8 T cells and mediators such as lymphotoxin in the pathogenesis of murine disease have been established. Experimental and human studies suggest vascular deposition of activated platelets may have a central role. Here, we review some recent advances in the understanding of severe malaria pathogenesis from human and animal studies, focusing on events at the level of the microcirculation, and highlight the role for activated host cells in initiating the pathology of the disease.</div>
</front>
</TEI>
<affiliations><list><country><li>Australie</li>
<li>France</li>
</country>
<region><li>Nouvelle-Galles du Sud</li>
<li>Provence-Alpes-Côte d'Azur</li>
<li>Victoria (État)</li>
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<settlement><li>Marseille</li>
<li>Melbourne</li>
<li>Sydney</li>
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<orgName><li>Université de Melbourne</li>
<li>Université de Sydney</li>
<li>Université de la Méditerranée</li>
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<tree><country name="Australie"><region name="Victoria (État)"><name sortKey="Rogerson, Stephen J" sort="Rogerson, Stephen J" uniqKey="Rogerson S" first="Stephen J" last="Rogerson">Stephen J. Rogerson</name>
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<name sortKey="Hunt, Nicholas H" sort="Hunt, Nicholas H" uniqKey="Hunt N" first="Nicholas H." last="Hunt">Nicholas H. Hunt</name>
<name sortKey="Hunt, Nicholas H" sort="Hunt, Nicholas H" uniqKey="Hunt N" first="Nicholas H." last="Hunt">Nicholas H. Hunt</name>
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<country name="France"><region name="Provence-Alpes-Côte d'Azur"><name sortKey="Grau, Georges E" sort="Grau, Georges E" uniqKey="Grau G" first="Georges E." last="Grau">Georges E. Grau</name>
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