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Hostile Takeover by Plasmodium: Reorganization of Parasite and Host Cell Membranes during Liver Stage Egress
The protozoan parasite Plasmodium is transmitted by female Anopheles mosquitoes and undergoes obligatory development within a parasitophorous vacuole in hepatocytes before it is released into the bloodstream. The transition to the blood stage was previously shown to involve the packaging of exoeryth...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Public Library of Science
2011
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3164640/ https://www.ncbi.nlm.nih.gov/pubmed/21909271 http://dx.doi.org/10.1371/journal.ppat.1002224 |
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author | Graewe, Stefanie Rankin, Kathleen E. Lehmann, Christine Deschermeier, Christina Hecht, Leonie Froehlke, Ulrike Stanway, Rebecca R. Heussler, Volker |
author_facet | Graewe, Stefanie Rankin, Kathleen E. Lehmann, Christine Deschermeier, Christina Hecht, Leonie Froehlke, Ulrike Stanway, Rebecca R. Heussler, Volker |
author_sort | Graewe, Stefanie |
collection | PubMed |
description | The protozoan parasite Plasmodium is transmitted by female Anopheles mosquitoes and undergoes obligatory development within a parasitophorous vacuole in hepatocytes before it is released into the bloodstream. The transition to the blood stage was previously shown to involve the packaging of exoerythrocytic merozoites into membrane-surrounded vesicles, called merosomes, which are delivered directly into liver sinusoids. However, it was unclear whether the membrane of these merosomes was derived from the parasite membrane, the parasitophorous vacuole membrane or the host cell membrane. This knowledge is required to determine how phagocytes will be directed against merosomes. Here, we fluorescently label the candidate membranes and use live cell imaging to show that the merosome membrane derives from the host cell membrane. We also demonstrate that proteins in the host cell membrane are lost during merozoite liberation from the parasitophorous vacuole. Immediately after the breakdown of the parasitophorous vacuole membrane, the host cell mitochondria begin to degenerate and protein biosynthesis arrests. The intact host cell plasma membrane surrounding merosomes allows Plasmodium to mask itself from the host immune system and bypass the numerous Kupffer cells on its way into the bloodstream. This represents an effective strategy for evading host defenses before establishing a blood stage infection. |
format | Online Article Text |
id | pubmed-3164640 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2011 |
publisher | Public Library of Science |
record_format | MEDLINE/PubMed |
spelling | pubmed-31646402011-09-09 Hostile Takeover by Plasmodium: Reorganization of Parasite and Host Cell Membranes during Liver Stage Egress Graewe, Stefanie Rankin, Kathleen E. Lehmann, Christine Deschermeier, Christina Hecht, Leonie Froehlke, Ulrike Stanway, Rebecca R. Heussler, Volker PLoS Pathog Research Article The protozoan parasite Plasmodium is transmitted by female Anopheles mosquitoes and undergoes obligatory development within a parasitophorous vacuole in hepatocytes before it is released into the bloodstream. The transition to the blood stage was previously shown to involve the packaging of exoerythrocytic merozoites into membrane-surrounded vesicles, called merosomes, which are delivered directly into liver sinusoids. However, it was unclear whether the membrane of these merosomes was derived from the parasite membrane, the parasitophorous vacuole membrane or the host cell membrane. This knowledge is required to determine how phagocytes will be directed against merosomes. Here, we fluorescently label the candidate membranes and use live cell imaging to show that the merosome membrane derives from the host cell membrane. We also demonstrate that proteins in the host cell membrane are lost during merozoite liberation from the parasitophorous vacuole. Immediately after the breakdown of the parasitophorous vacuole membrane, the host cell mitochondria begin to degenerate and protein biosynthesis arrests. The intact host cell plasma membrane surrounding merosomes allows Plasmodium to mask itself from the host immune system and bypass the numerous Kupffer cells on its way into the bloodstream. This represents an effective strategy for evading host defenses before establishing a blood stage infection. Public Library of Science 2011-09-01 /pmc/articles/PMC3164640/ /pubmed/21909271 http://dx.doi.org/10.1371/journal.ppat.1002224 Text en Graewe et al. http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited. |
spellingShingle | Research Article Graewe, Stefanie Rankin, Kathleen E. Lehmann, Christine Deschermeier, Christina Hecht, Leonie Froehlke, Ulrike Stanway, Rebecca R. Heussler, Volker Hostile Takeover by Plasmodium: Reorganization of Parasite and Host Cell Membranes during Liver Stage Egress |
title | Hostile Takeover by Plasmodium: Reorganization of Parasite and Host Cell Membranes during Liver Stage Egress |
title_full | Hostile Takeover by Plasmodium: Reorganization of Parasite and Host Cell Membranes during Liver Stage Egress |
title_fullStr | Hostile Takeover by Plasmodium: Reorganization of Parasite and Host Cell Membranes during Liver Stage Egress |
title_full_unstemmed | Hostile Takeover by Plasmodium: Reorganization of Parasite and Host Cell Membranes during Liver Stage Egress |
title_short | Hostile Takeover by Plasmodium: Reorganization of Parasite and Host Cell Membranes during Liver Stage Egress |
title_sort | hostile takeover by plasmodium: reorganization of parasite and host cell membranes during liver stage egress |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3164640/ https://www.ncbi.nlm.nih.gov/pubmed/21909271 http://dx.doi.org/10.1371/journal.ppat.1002224 |
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