Host scavenger receptor SR-BI plays a dual role in the establishment of malaria parasite liver infection
An obligatory step of malaria parasite infection is Plasmodium sporozoite invasion of host hepatocytes, and host lipoprotein clearance pathways have been linked to Plasmodium liver infection. By using RNA interference to screen lipoprotein-related host factors, we show here that the class B, type I...
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| Veröffentlicht in: | Cell host & microbe 2008-09, Vol.4 (3), p.271-282 |
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| creator | Rodrigues, Cristina D Hannus, Michael Prudêncio, Miguel Martin, Cécilie Gonçalves, Lígia A Portugal, Sílvia Epiphanio, Sabrina Akinc, Akin Hadwiger, Philipp Jahn-Hofmann, Kerstin Röhl, Ingo van Gemert, Geert-Jan Franetich, Jean-François Luty, Adrian J F Sauerwein, Robert Mazier, Dominique Koteliansky, Victor Vornlocher, Hans-Peter Echeverri, Christophe J Mota, Maria M |
| description | An obligatory step of malaria parasite infection is Plasmodium sporozoite invasion of host hepatocytes, and host lipoprotein clearance pathways have been linked to Plasmodium liver infection. By using RNA interference to screen lipoprotein-related host factors, we show here that the class B, type I scavenger receptor (SR-BI) is the strongest regulator of Plasmodium infection among these factors. Inhibition of SR-BI function reduced P. berghei infection in Huh7 cells, and overexpression of SR-BI led to increased infection. In vivo silencing of liver SR-BI expression in mice and inhibition of SR-BI activity in human primary hepatocytes reduced infection by P. berghei and by P. falciparum, respectively. Heterozygous SR-BI(+/-) mice displayed reduced P. berghei infection rates correlating with liver SR-BI expression levels. Additional analyses revealed that SR-BI plays a dual role in Plasmodium infection, affecting both sporozoite invasion and intracellular parasite development, and may therefore constitute a good target for malaria prophylaxis. |
| doi_str_mv | 10.1016/j.chom.2008.07.012 |
| format | Article |
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By using RNA interference to screen lipoprotein-related host factors, we show here that the class B, type I scavenger receptor (SR-BI) is the strongest regulator of Plasmodium infection among these factors. Inhibition of SR-BI function reduced P. berghei infection in Huh7 cells, and overexpression of SR-BI led to increased infection. In vivo silencing of liver SR-BI expression in mice and inhibition of SR-BI activity in human primary hepatocytes reduced infection by P. berghei and by P. falciparum, respectively. Heterozygous SR-BI(+/-) mice displayed reduced P. berghei infection rates correlating with liver SR-BI expression levels. Additional analyses revealed that SR-BI plays a dual role in Plasmodium infection, affecting both sporozoite invasion and intracellular parasite development, and may therefore constitute a good target for malaria prophylaxis.</abstract><cop>United States</cop><pmid>18779053</pmid><doi>10.1016/j.chom.2008.07.012</doi><tpages>12</tpages><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; Cell Press Free Archives; Elsevier ScienceDirect Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals |
| subjects | Animals Cell Line Cells, Cultured Hepatocytes - metabolism Hepatocytes - parasitology Host-Parasite Interactions Humans Liver Diseases - metabolism Liver Diseases - parasitology Malaria - metabolism Malaria - parasitology Mice Mice, Knockout Plasmodium Plasmodium - pathogenicity Plasmodium - physiology Plasmodium falciparum Scavenger Receptors, Class B - genetics Scavenger Receptors, Class B - metabolism Vacuoles - metabolism Vacuoles - parasitology |
| title | Host scavenger receptor SR-BI plays a dual role in the establishment of malaria parasite liver infection |
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