Parasitophorous vacuole

After binding, T. cruzi enters host cells via an acidic vacuole, which fuses with lysosomes [818,844-846]. The parasitophorous vacuole formed in this way is later disrupted in order to release the trypanosomes into the cytosol. 7ra j-sialidase activity seems to be required for the latter step, as it desialylates the highly sialylated lysosomal... 

Maier, A. G., Rug, M., O Neill, M. T., Beeson, J. G., Marti, M., Reeder, J., and Cowman, A. F. (2007). Skeleton-binding protein 1 functions at the parasitophorous vacuole membrane to traffic PfEMPl to the Plasmodium falciparum-infected erythrocyte surface. Blood 109, 1289-1297. 

Nyalwidhe, J. and Lingelbach, K. (2006). Proteases and chaperones are the most abundant proteins in the parasitophorous vacuole of Plasmodium falciparum-infected erythrocytes. Proteomics 6,1563-1573. 

Ultrastructural observations suggested that during invasion Plasmodium rhoptries extrude copious membranous material (see ref. 6 and references therein), which may provide a matrix for rhoptry proteins (13). Some rhoptry proteins bind to both erythrocyte inside-out vesicles and to vesicles prepared from phospholipids predominant in the erythrocyte membrane inner leaflet, particularly phosphatidylserine (PS) and phosphatidylinositol (PI) (14,15). One has been shown to intercalate into the erythrocyte membrane (16). These proteins, the RHOP-H complex and SERA, are proposed to integrate differentially into the erythrocyte membrane upon invasion, causing an inward membrane expansion, to produce the parasitophorous vacuole. 

On balance, the evidence points to rhoptry lipids being involved, at the least, in sequestering proteins which, upon introduction into the erythrocyte membrane with or without rhoptry lipids, are directly responsible for the destabilization of the erythrocyte membrane, and subsequent parasitophorous vacuole membrane formation. Whether rhoptry lipids actually become an integral part of the parasitophorous vacuole membrane, wholly or in combination with erythrocyte lipids, is not clear. Rhoptry lipids probably combine directly with erythrocyte lipids in the parasitophorous vacuole membrane. 

A parasite phospholipase (most likely PLA2) may participate in host cell invasion by T. gondii (21). The presumptive PLAj enhanced host cell invasion. Phospholipase has been shown to solubilize rhoptry proteins of P. falciparum presumably involved in erythrocyte invasion (22). Solubilization of internal, latent, membrane-bound rhoptry proteins by lipid degradation may be a general method in the Apicomplexa for initiating active host cell penetration and parasitophorous vacuole membrane formation after attachment. 

Thus, the infected erythrocyte has access to host plasma lipids, predominantly from HDL. Further, the HDL, or its lipids, must be transported from the erythrocyte membrane and through the parasitophorous vacuole membrane to the developing parasite (for review see ref. 29). The importance of this for Plasmodium is illustrated by the work of Grellier et al. (30) who showed that HDL alone supports the differentiation and multiplication of the parasite. Very low density lipoproteins (VLDL), low density lipoproteins (LDL) or apolipoproteins do not support complete schizogony and... 

Joiner, K. A. (1991) Rhoptry lipids and parasitophorous vacuole formation — a slippery issue. Parasitol. Today 7 226-227. 

Ward, G. E., Miller, L. H. and Dvorak, J. A. (1993) The origin of parasitophorous vacuole membrane lipids in malaria-infected erythrocytes. J. Cell Sci. 106 237-248. 

J. F. (1994) Structure and function of the parasitophorous vacuole membrane surrounding Toxoplasma gondii. Ann. NY Acad. Sci. 730 1-6. 

Halonen, S. K. and Weidner, E. (1994) Overcoating of Toxoplasma parasitophorous vacuoles with host cell vimentin type intermediate filaments. J. Euk. Microbiol. 41 65-71. 

Following invasion of their host cell, several intracellular parasites remain inside the parasitophorous vacuole which may or may not fuse with lysosomes. Other pathogens, such as Rickettsia spp. Listeria monocytogenes. Shigellaflexneri, Theileria parva, Babesia bovis and Trypanosoma cruzi must leave the phagocytic vacuole and establish themselves into the cytosolic compartment to survive successfully. Obviously, disruption of the phagocytic vacuole represents a critical step in this escape process (reviewed in ref. 34). The role of a hemolysin secreted by T. cruzi amastigotes is discussed in this section. 

In T. cru2 -infected macrophages, the hemolysin was localized inside the luminal space and closely apposed to the phagosome membrane (36), indicating that it is secreted into the acidic phagosome. Finally, the observation that the exit of T. cruzi from the phagosomes is inhibited by drugs that raise the pH of the intracellular compartment supports the notion that the acid-active hemolysin is involved in the destruction of the parasitophorous vacuoles, and hence allows the parasite to multiply in the appropriate compartment. 

Joiner, K. A., Furhman, S. A., Miettinen, H. M., Kasper, L. H. and Mellman, I. (1990) Toxoplasma gondii—fusion competence of parasitophorous vacuoles in Fc receptor transfected fibroblasts. Science 249 641-646. 

Entzeroth, R., Dubremetz, J. F., Hodick, D. and Ferreira, E. (1986) Immunoelectromicro-scopic demonstration of the exocytosis of dense granules contents into the secondary parasitophorous vacuole of Sarcocystis muris (Protozoa, Apicomplexa). Eur. J. Cell Biol. 41 182-188. 

Achbarou, A., Mercereau-Puijalon, O., Sadak, A. et al. (1991) Differential targeting of dense granules proteins in the parasitophorous vacuole of Toxoplasma gondii. Parasitology 103 321-329. 

Antonine, J. C., Prina, E., Jouanne, C. and Bongrand, P. (1990) Parasitophorous vacuoles of Leishmania amazonensis- mkcted macrophages maintain an acidic pH. Infect. Immun. 58 779-787. 

Rabinovitch, M., Topper, G., Cristello, P. and Rich, A. (1985) Receptor-mediated entry of peroxidases into the parasitophorous vacuole of macrophages infected with Leishmania mexicana amazonensis. J. Leuk. Biol. 31 247-261. 

Heinzen, R. A., Scidmore, M. A., Rockey, D. D and Hackstadt, T. (1996) Differential interaction with endocytic and exocytic pathways distinguish parasitophorous vacuoles of Coxiella burnetii and Chlamydia trachomatis. Infect. Immun. 64, 796-809. 

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