The homeostasis of Plasmodium falciparum-infected red blood cells.

The asexual reproduction cycle of Plasmodium falciparum, the parasite responsible for severe malaria, occurs within red blood cells. A merozoite invades a red cell in the circulation, develops and multiplies, and after about 48 hours ruptures the host cell, releasing 15-32 merozoites ready to invade...

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Autores principales:	Jakob M A Mauritz, Alessandro Esposito, Hagai Ginsburg, Clemens F Kaminski, Teresa Tiffert, Virgilio L Lew
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2009
Materias:	Biology (General) QH301-705.5
Acceso en línea:	https://doaj.org/article/2f68b2db85a2472c9d176fca71436a17
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spelling	oai:doaj.org-article:2f68b2db85a2472c9d176fca71436a172021-11-25T05:41:44ZThe homeostasis of Plasmodium falciparum-infected red blood cells.1553-734X1553-735810.1371/journal.pcbi.1000339https://doaj.org/article/2f68b2db85a2472c9d176fca71436a172009-04-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/19343220/?tool=EBIhttps://doaj.org/toc/1553-734Xhttps://doaj.org/toc/1553-7358The asexual reproduction cycle of Plasmodium falciparum, the parasite responsible for severe malaria, occurs within red blood cells. A merozoite invades a red cell in the circulation, develops and multiplies, and after about 48 hours ruptures the host cell, releasing 15-32 merozoites ready to invade new red blood cells. During this cycle, the parasite increases the host cell permeability so much that when similar permeabilization was simulated on uninfected red cells, lysis occurred before approximately 48 h. So how could infected cells, with a growing parasite inside, prevent lysis before the parasite has completed its developmental cycle? A mathematical model of the homeostasis of infected red cells suggested that it is the wasteful consumption of host cell hemoglobin that prevents early lysis by the progressive reduction in the colloid-osmotic pressure within the host (the colloid-osmotic hypothesis). However, two critical model predictions, that infected cells would swell to near prelytic sphericity and that the hemoglobin concentration would become progressively reduced, remained controversial. In this paper, we are able for the first time to correlate model predictions with recent experimental data in the literature and explore the fine details of the homeostasis of infected red blood cells during five model-defined periods of parasite development. The conclusions suggest that infected red cells do reach proximity to lytic rupture regardless of their actual volume, thus requiring a progressive reduction in their hemoglobin concentration to prevent premature lysis.Jakob M A MauritzAlessandro EspositoHagai GinsburgClemens F KaminskiTeresa TiffertVirgilio L LewPublic Library of Science (PLoS)articleBiology (General)QH301-705.5ENPLoS Computational Biology, Vol 5, Iss 4, p e1000339 (2009)
institution	DOAJ
collection	DOAJ
language	EN
topic	Biology (General) QH301-705.5
spellingShingle	Biology (General) QH301-705.5 Jakob M A Mauritz Alessandro Esposito Hagai Ginsburg Clemens F Kaminski Teresa Tiffert Virgilio L Lew The homeostasis of Plasmodium falciparum-infected red blood cells.
description	The asexual reproduction cycle of Plasmodium falciparum, the parasite responsible for severe malaria, occurs within red blood cells. A merozoite invades a red cell in the circulation, develops and multiplies, and after about 48 hours ruptures the host cell, releasing 15-32 merozoites ready to invade new red blood cells. During this cycle, the parasite increases the host cell permeability so much that when similar permeabilization was simulated on uninfected red cells, lysis occurred before approximately 48 h. So how could infected cells, with a growing parasite inside, prevent lysis before the parasite has completed its developmental cycle? A mathematical model of the homeostasis of infected red cells suggested that it is the wasteful consumption of host cell hemoglobin that prevents early lysis by the progressive reduction in the colloid-osmotic pressure within the host (the colloid-osmotic hypothesis). However, two critical model predictions, that infected cells would swell to near prelytic sphericity and that the hemoglobin concentration would become progressively reduced, remained controversial. In this paper, we are able for the first time to correlate model predictions with recent experimental data in the literature and explore the fine details of the homeostasis of infected red blood cells during five model-defined periods of parasite development. The conclusions suggest that infected red cells do reach proximity to lytic rupture regardless of their actual volume, thus requiring a progressive reduction in their hemoglobin concentration to prevent premature lysis.
format	article
author	Jakob M A Mauritz Alessandro Esposito Hagai Ginsburg Clemens F Kaminski Teresa Tiffert Virgilio L Lew
author_facet	Jakob M A Mauritz Alessandro Esposito Hagai Ginsburg Clemens F Kaminski Teresa Tiffert Virgilio L Lew
author_sort	Jakob M A Mauritz
title	The homeostasis of Plasmodium falciparum-infected red blood cells.
title_short	The homeostasis of Plasmodium falciparum-infected red blood cells.
title_full	The homeostasis of Plasmodium falciparum-infected red blood cells.
title_fullStr	The homeostasis of Plasmodium falciparum-infected red blood cells.
title_full_unstemmed	The homeostasis of Plasmodium falciparum-infected red blood cells.
title_sort	homeostasis of plasmodium falciparum-infected red blood cells.
publisher	Public Library of Science (PLoS)
publishDate	2009
url	https://doaj.org/article/2f68b2db85a2472c9d176fca71436a17
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The homeostasis of Plasmodium falciparum-infected red blood cells.

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