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...

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Autores principales: Stefanie Graewe, Kathleen E Rankin, Christine Lehmann, Christina Deschermeier, Leonie Hecht, Ulrike Froehlke, Rebecca R Stanway, Volker Heussler
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Publicado: Public Library of Science (PLoS) 2011
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spelling oai:doaj.org-article:d1555e3cf0184a8e818e7c6ccdc5996f2021-11-18T06:03:01ZHostile takeover by Plasmodium: reorganization of parasite and host cell membranes during liver stage egress.1553-73661553-737410.1371/journal.ppat.1002224https://doaj.org/article/d1555e3cf0184a8e818e7c6ccdc5996f2011-09-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/21909271/?tool=EBIhttps://doaj.org/toc/1553-7366https://doaj.org/toc/1553-7374The 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.Stefanie GraeweKathleen E RankinChristine LehmannChristina DeschermeierLeonie HechtUlrike FroehlkeRebecca R StanwayVolker HeusslerPublic Library of Science (PLoS)articleImmunologic diseases. AllergyRC581-607Biology (General)QH301-705.5ENPLoS Pathogens, Vol 7, Iss 9, p e1002224 (2011)
institution DOAJ
collection DOAJ
language EN
topic Immunologic diseases. Allergy
RC581-607
Biology (General)
QH301-705.5
spellingShingle Immunologic diseases. Allergy
RC581-607
Biology (General)
QH301-705.5
Stefanie Graewe
Kathleen E Rankin
Christine Lehmann
Christina Deschermeier
Leonie Hecht
Ulrike Froehlke
Rebecca R Stanway
Volker Heussler
Hostile takeover by Plasmodium: reorganization of parasite and host cell membranes during liver stage egress.
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 article
author Stefanie Graewe
Kathleen E Rankin
Christine Lehmann
Christina Deschermeier
Leonie Hecht
Ulrike Froehlke
Rebecca R Stanway
Volker Heussler
author_facet Stefanie Graewe
Kathleen E Rankin
Christine Lehmann
Christina Deschermeier
Leonie Hecht
Ulrike Froehlke
Rebecca R Stanway
Volker Heussler
author_sort Stefanie Graewe
title 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_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_sort hostile takeover by plasmodium: reorganization of parasite and host cell membranes during liver stage egress.
publisher Public Library of Science (PLoS)
publishDate 2011
url https://doaj.org/article/d1555e3cf0184a8e818e7c6ccdc5996f
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