Lipid transport in Plasmodium.

During intraerythrocytic development, the human malaria parasite Plasmodium falciparum actively internalizes phospholipids from its erythrocyte membrane and the extracellular medium. The import of exogenous lipids is not due to endocytosis, but to energy-dependent, transbilayer movement of phospholipids induced by the parasite in the erythrocyte surface. Novel tubular membranes that appear to emerge from the vacuole of the parasite and extend into the erythrocyte cytoplasm are labeled by exogenously added fluorescent lipids. These tubules interact with the erythrocyte membrane, but definitive evidence for their role in catalyzing transbilayer phospholipid movement in the red blood cell bilayer is still not available. Both biochemical and microscopic studies indicate that all lipid analogs internalized into the intraerythrocytic compartments and/or the parasite are not exported back to the host cell surface. Nonexchangeable fluorescent lipids are exported from a parasite to its intraerythrocytic tubules, but not to an adjacent parasite in a double-infected red blood cell. Thus, while the intraerythrocytic membranes engage in prominent tubular development at the vacuolar surface and deliver lipids to the parasite they originate from, they appear to be incapable of vesicular or tubular membrane export across the erythrocyte cytosol. Parasite Golgi activities for the synthesis and accumulation of sphingomyelin are detected in the intraerythrocytic tubules, indicating a novel export of classic secretory functions to their lumen, which could be central to both tubular development and lipid-sorting activities in these organelles.