Malaria Parasites Hijack Host Receptors From Exosomes to Capture Lipoproteins

Malaria parasites cannot multiply in host erythrocytes without cholesterol because they lack complete sterol biosynthesis systems. This suggests parasitized red blood cells (pRBCs) need to capture host sterols, but its mechanism remains unknown. Here we identified a novel high-density lipoprotein (H...

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Autores principales:	Naoyuki Iso-o, Keisuke Komatsuya, Fuyuki Tokumasu, Noriko Isoo, Tomohiro Ishigaki, Hiroshi Yasui, Hiroshi Yotsuyanagi, Masumi Hara, Kiyoshi Kita
Formato:	article
Lenguaje:	EN
Publicado:	Frontiers Media S.A. 2021
Materias:	malaria plasmodium falciparum cholesterol lipoproteins lipid exosomes Biology (General) QH301-705.5
Acceso en línea:	https://doaj.org/article/35b4fa923b6744ca8196c1975c19e9bb
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spelling	oai:doaj.org-article:35b4fa923b6744ca8196c1975c19e9bb2021-11-11T06:33:15ZMalaria Parasites Hijack Host Receptors From Exosomes to Capture Lipoproteins2296-634X10.3389/fcell.2021.749153https://doaj.org/article/35b4fa923b6744ca8196c1975c19e9bb2021-11-01T00:00:00Zhttps://www.frontiersin.org/articles/10.3389/fcell.2021.749153/fullhttps://doaj.org/toc/2296-634XMalaria parasites cannot multiply in host erythrocytes without cholesterol because they lack complete sterol biosynthesis systems. This suggests parasitized red blood cells (pRBCs) need to capture host sterols, but its mechanism remains unknown. Here we identified a novel high-density lipoprotein (HDL)-delivery pathway operating in blood-stage Plasmodium. In parasitized mouse plasma, exosomes positive for scavenger receptor CD36 and platelet-specific CD41 increased. These CDs were detected in pRBCs and internal parasites. A low molecular antagonist for scavenger receptors, BLT-1, blocked HDL uptake to pRBCs and suppressed Plasmodium growth in vitro. Furthermore, platelet-derived exosomes were internalized in pRBCs. Thus, we presume CD36 is delivered to malaria parasites from platelets by exosomes, which enables parasites to steal HDL for cholesterol supply. Cholesterol needs to cross three membranes (RBC, parasitophorous vacuole and parasite’s plasma membranes) to reach parasite, but our findings can explain the first step of sterol uptake by intracellular parasites.Naoyuki Iso-oNaoyuki Iso-oKeisuke KomatsuyaKeisuke KomatsuyaFuyuki TokumasuFuyuki TokumasuNoriko IsooTomohiro IshigakiHiroshi YasuiHiroshi YotsuyanagiMasumi HaraKiyoshi KitaKiyoshi KitaKiyoshi KitaFrontiers Media S.A.articlemalariaplasmodium falciparumcholesterollipoproteinslipidexosomesBiology (General)QH301-705.5ENFrontiers in Cell and Developmental Biology, Vol 9 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	malaria plasmodium falciparum cholesterol lipoproteins lipid exosomes Biology (General) QH301-705.5
spellingShingle	malaria plasmodium falciparum cholesterol lipoproteins lipid exosomes Biology (General) QH301-705.5 Naoyuki Iso-o Naoyuki Iso-o Keisuke Komatsuya Keisuke Komatsuya Fuyuki Tokumasu Fuyuki Tokumasu Noriko Isoo Tomohiro Ishigaki Hiroshi Yasui Hiroshi Yotsuyanagi Masumi Hara Kiyoshi Kita Kiyoshi Kita Kiyoshi Kita Malaria Parasites Hijack Host Receptors From Exosomes to Capture Lipoproteins
description	Malaria parasites cannot multiply in host erythrocytes without cholesterol because they lack complete sterol biosynthesis systems. This suggests parasitized red blood cells (pRBCs) need to capture host sterols, but its mechanism remains unknown. Here we identified a novel high-density lipoprotein (HDL)-delivery pathway operating in blood-stage Plasmodium. In parasitized mouse plasma, exosomes positive for scavenger receptor CD36 and platelet-specific CD41 increased. These CDs were detected in pRBCs and internal parasites. A low molecular antagonist for scavenger receptors, BLT-1, blocked HDL uptake to pRBCs and suppressed Plasmodium growth in vitro. Furthermore, platelet-derived exosomes were internalized in pRBCs. Thus, we presume CD36 is delivered to malaria parasites from platelets by exosomes, which enables parasites to steal HDL for cholesterol supply. Cholesterol needs to cross three membranes (RBC, parasitophorous vacuole and parasite’s plasma membranes) to reach parasite, but our findings can explain the first step of sterol uptake by intracellular parasites.
format	article
author	Naoyuki Iso-o Naoyuki Iso-o Keisuke Komatsuya Keisuke Komatsuya Fuyuki Tokumasu Fuyuki Tokumasu Noriko Isoo Tomohiro Ishigaki Hiroshi Yasui Hiroshi Yotsuyanagi Masumi Hara Kiyoshi Kita Kiyoshi Kita Kiyoshi Kita
author_facet	Naoyuki Iso-o Naoyuki Iso-o Keisuke Komatsuya Keisuke Komatsuya Fuyuki Tokumasu Fuyuki Tokumasu Noriko Isoo Tomohiro Ishigaki Hiroshi Yasui Hiroshi Yotsuyanagi Masumi Hara Kiyoshi Kita Kiyoshi Kita Kiyoshi Kita
author_sort	Naoyuki Iso-o
title	Malaria Parasites Hijack Host Receptors From Exosomes to Capture Lipoproteins
title_short	Malaria Parasites Hijack Host Receptors From Exosomes to Capture Lipoproteins
title_full	Malaria Parasites Hijack Host Receptors From Exosomes to Capture Lipoproteins
title_fullStr	Malaria Parasites Hijack Host Receptors From Exosomes to Capture Lipoproteins
title_full_unstemmed	Malaria Parasites Hijack Host Receptors From Exosomes to Capture Lipoproteins
title_sort	malaria parasites hijack host receptors from exosomes to capture lipoproteins
publisher	Frontiers Media S.A.
publishDate	2021
url	https://doaj.org/article/35b4fa923b6744ca8196c1975c19e9bb
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Malaria Parasites Hijack Host Receptors From Exosomes to Capture Lipoproteins

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