期刊
FRONTIERS IN CELL AND DEVELOPMENTAL BIOLOGY
卷 9, 期 -, 页码 -出版社
FRONTIERS MEDIA SA
DOI: 10.3389/fcell.2021.749153
关键词
malaria; plasmodium falciparum; cholesterol; lipoproteins; lipid; exosomes; scavenger receptors
资金
- (KAKENHI). Grant [17K08805, 26461499, 17K10014]
- University of Tokyo
- Shimadzu Corporation, and Department of Cellular Architecture Studies, Institute of Tropical Medicine, Nagasaki University
- SHIONOGI
- Grants-in-Aid for Scientific Research [26461499, 17K10014, 17K08805] Funding Source: KAKEN
Malaria parasites require host cholesterol for multiplication in erythrocytes, and a novel HDL-delivery pathway involving exosomes and scavenger receptors may facilitate this process. Platelet-derived exosomes containing CD36 can potentially deliver cholesterol to parasites, explaining the first step of sterol uptake by intracellular parasites.
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.
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