Merozoite release from Plasmodium falciparum-infected erythrocytes involves the transfer of DiIC16 from infected cell membrane to Maurer’s clefts

Abstract

Merozoite release from infected erythrocytes is a complex process, which is still not fully understood. Such process was characterised at ultra-structural level in this work by labelling erythrocyte membrane with a fluorescent lipid probe and subsequent photo-conversion into an electron-dense precipitate. A lipophilic DiIC16 probe was inserted into the infected erythrocyte surface and the transport of this phospholipid analogue through the erythrocyte membrane was followed up during 48 h of the asexual erythrocyte cycle. The lipid probe was transferred from infected erythrocyte membranes to Maurer’s clefts during merozoite release, thereby indicating that these membranes remained inside host cells after parasite release. Fluorescent structures were never observed inside infected erythrocytes preceding merozoite exit and merozoites released from infected erythrocyte were not fluorescent. However, specific precipitated material was localised bordering the parasitophorous vacuole membrane and tubovesicular membranes when labelled non-infected erythrocytes were invaded by merozoites. It was revealed that lipids were interchangeable from one membrane to another, passing from infected erythrocyte membrane to Maurer’s clefts inside the erythrocyte ghost, even after merozoite release. Maurer’s clefts became photo-converted following merozoite release, suggesting that these structures were in close contact with infected erythrocyte membrane during merozoite exit and possibly played some role in malarial parasite exit from the host cell.Electronic supplementary materialThe online version of this article (doi:10.1007/s00436-011-2314-7) contains supplementary material, which is available to authorized users.

Plasmodium falciparum infection-induced changes in erythrocyte membrane proteins

“…P. falciparum parasites are known to extensively remodel host cells after the formation of a PV at the time of RBC invasion by merozoites. The PVM is composed of host detergent-resistant membrane proteins that are present in lipid rafts on the RBC plasma membrane (Murphy et al 2004(Murphy et al , 2007Salzer and Prohaska 2001;Cortes et al 2011). As membrane invagination is not a common feature in healthy erythrocytes, up-represented H. sapiens proteins in iRBC samples might result from the recruitment of cytosolic host proteins by the parasite to establish the host-parasite interfaces that extend into the erythrocyte cytoplasm.…”