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Adhesion of Plasmodium falciparum-infected erythrocytes to human cells: molecular mechanisms and therapeutic implications

Severe malaria has a high mortality rate (15–20%) despite treatment with effective antimalarial drugs. Adjunctive therapies for severe malaria that target the underlying disease process are therefore urgently required. Adhesion of erythrocytes infected with Plasmodium falciparum to human cells has a...

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Detalles Bibliográficos
Autores principales: Rowe, J. Alexandra, Claessens, Antoine, Corrigan, Ruth A., Arman, Mònica
Formato: Texto
Lenguaje:English
Publicado: Cambridge University Press 2009
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2878476/
https://www.ncbi.nlm.nih.gov/pubmed/19467172
http://dx.doi.org/10.1017/S1462399409001082
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author Rowe, J. Alexandra
Claessens, Antoine
Corrigan, Ruth A.
Arman, Mònica
author_facet Rowe, J. Alexandra
Claessens, Antoine
Corrigan, Ruth A.
Arman, Mònica
author_sort Rowe, J. Alexandra
collection PubMed
description Severe malaria has a high mortality rate (15–20%) despite treatment with effective antimalarial drugs. Adjunctive therapies for severe malaria that target the underlying disease process are therefore urgently required. Adhesion of erythrocytes infected with Plasmodium falciparum to human cells has a key role in the pathogenesis of life-threatening malaria and could be targeted with antiadhesion therapy. Parasite adhesion interactions include binding to endothelial cells (cytoadherence), rosetting with uninfected erythrocytes and platelet-mediated clumping of infected erythrocytes. Recent research has started to define the molecular mechanisms of parasite adhesion, and antiadhesion therapies are being explored. However, many fundamental questions regarding the role of parasite adhesion in severe malaria remain unanswered. There is strong evidence that rosetting contributes to severe malaria in sub-Saharan Africa; however, the identity of other parasite adhesion phenotypes that are implicated in disease pathogenesis remains unclear. In addition, the possibility of geographic variation in adhesion phenotypes causing severe malaria, linked to differences in malaria transmission levels and host immunity, has been neglected. Further research is needed to realise the untapped potential of antiadhesion adjunctive therapies, which could revolutionise the treatment of severe malaria and reduce the high mortality rate of the disease.
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spelling pubmed-28784762010-05-29 Adhesion of Plasmodium falciparum-infected erythrocytes to human cells: molecular mechanisms and therapeutic implications Rowe, J. Alexandra Claessens, Antoine Corrigan, Ruth A. Arman, Mònica Expert Rev Mol Med Review Article Severe malaria has a high mortality rate (15–20%) despite treatment with effective antimalarial drugs. Adjunctive therapies for severe malaria that target the underlying disease process are therefore urgently required. Adhesion of erythrocytes infected with Plasmodium falciparum to human cells has a key role in the pathogenesis of life-threatening malaria and could be targeted with antiadhesion therapy. Parasite adhesion interactions include binding to endothelial cells (cytoadherence), rosetting with uninfected erythrocytes and platelet-mediated clumping of infected erythrocytes. Recent research has started to define the molecular mechanisms of parasite adhesion, and antiadhesion therapies are being explored. However, many fundamental questions regarding the role of parasite adhesion in severe malaria remain unanswered. There is strong evidence that rosetting contributes to severe malaria in sub-Saharan Africa; however, the identity of other parasite adhesion phenotypes that are implicated in disease pathogenesis remains unclear. In addition, the possibility of geographic variation in adhesion phenotypes causing severe malaria, linked to differences in malaria transmission levels and host immunity, has been neglected. Further research is needed to realise the untapped potential of antiadhesion adjunctive therapies, which could revolutionise the treatment of severe malaria and reduce the high mortality rate of the disease. Cambridge University Press 2009-05 2009-05 /pmc/articles/PMC2878476/ /pubmed/19467172 http://dx.doi.org/10.1017/S1462399409001082 Text en Copyright © Cambridge University Press 2009 http://creativecommons.org/licenses/by-nc-sa/2.5/ The online version of this article is published within an Open Access environment subject to the conditions of the Creative Commons Attribution-NonCommercial-ShareAlike licence <http://creativecommons.org/licenses/by-nc-sa/2.5/>. (http://creativecommons.org/licenses/by-nc-sa/2.5/>) The written permission of Cambridge University Press must be obtained for commercial re-use
spellingShingle Review Article
Rowe, J. Alexandra
Claessens, Antoine
Corrigan, Ruth A.
Arman, Mònica
Adhesion of Plasmodium falciparum-infected erythrocytes to human cells: molecular mechanisms and therapeutic implications
title Adhesion of Plasmodium falciparum-infected erythrocytes to human cells: molecular mechanisms and therapeutic implications
title_full Adhesion of Plasmodium falciparum-infected erythrocytes to human cells: molecular mechanisms and therapeutic implications
title_fullStr Adhesion of Plasmodium falciparum-infected erythrocytes to human cells: molecular mechanisms and therapeutic implications
title_full_unstemmed Adhesion of Plasmodium falciparum-infected erythrocytes to human cells: molecular mechanisms and therapeutic implications
title_short Adhesion of Plasmodium falciparum-infected erythrocytes to human cells: molecular mechanisms and therapeutic implications
title_sort adhesion of plasmodium falciparum-infected erythrocytes to human cells: molecular mechanisms and therapeutic implications
topic Review Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2878476/
https://www.ncbi.nlm.nih.gov/pubmed/19467172
http://dx.doi.org/10.1017/S1462399409001082
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