Is Toxoplasma egress the first step in invasion?

Hoff, Eleanor F; Carruthers, Vern B.

doi:10.1016/s1471-4922(02)02240-7

Cited by 73 publications

(52 citation statements)

References 34 publications

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“…The mechanism leading to egress of parasites from infected cells is still poorly understood, but it does share some common features with the process of invasion [10]. In P. falciparum, the process of merozoite release was recently examined using parasite lines expressing green fluorescent protein (GFP) fused to proteins targeted to the parasitophorous vacuole and the host erythrocyte cytosol.…”

Section: Host Cell Invasion Parasitophorous Vacuole Formation and Egmentioning

confidence: 99%

Molecular and functional aspects of parasite invasion

Soldati

Foth

Cowman

2004

Trends in Parasitology

109

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Apicomplexan parasites have evolved an efficient mechanism to gain entry into non-phagocytic cells, hence challenging their hosts by the establishment of infection in immuno-privileged tissues. Gliding motility is a prerequisite for the invasive stage of most apicomplexans, allowing them to migrate across tissues, and actively invade and egress host cells. In the late 1960s, detailed morphological studies revealed that motile apicomplexans share an elaborate architecture comprising a subpellicular cytoskeleton and apical organelles. Since 1993, the development of technologies for transient and stable transfection have provided powerful tools with which to identify gene products associated with these structures and organelles, as well as to understand their functions. In combination with access to several parasite genomes, it is now possible to compare and contrast the strategies and molecular machines that have been selectively designed by distinct life stages within a species, or by different apicomplexan species, to optimize infection

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Section: Host Cell Invasion Parasitophorous Vacuole Formation and Egmentioning

confidence: 99%

Molecular and functional aspects of parasite invasion

Soldati

Foth

Cowman

2004

Trends in Parasitology

109

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“…Transient rises in intracellular calcium within tachyzoites serve as a trigger for parasite egress from host cells and participate in the cell gliding motility and host-cell invasion processes critical to T. gondii survival (Hoff and Carruthers, 2002;Nagamune et al, 2008;Chandramohanadas et al, 2009;Lourido et al, 2010). Calcium binding activates calmodulin and downstream calmodulin-dependent protein kinases have been implicated in life-cycle and erythrocyte invasion of the apicomplexan, Plasmodium falciparum (Vaid et al, 2008;Wurtz et al, 2009), but these pathways are not well understood in T. gondii.…”

mentioning

confidence: 99%

Evaluation of Five Antischizophrenic Agents Against Toxoplasma gondii in Human Cell Cultures

Goodwin

Strobl

Lindsay

2011

Journal of Parasitology

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“…3B), (ii) fewer E. tenella sporozoites were found inside epithelial cells in coccidian-immunized chickens than in naive animals (30), and (iii) externally triggered egress was the major fate of T. gondii during acute infection (36). In the case of Toxoplasma infection, PLC and other Ca 2ϩ -related molecules are critical mediators of parasite egress (2,12,26). This process is thought to involve an as yet unidentified parasite sensor that detects changes in intracellular Ca 2ϩ levels.…”

Section: Discussionmentioning

confidence: 99%

Enhanced Egress of Intracellular Eimeria tenella Sporozoites by Splenic Lymphocytes from Coccidian-Infected Chickens

et al. 2011

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Egress, which describes the mechanism that some intracellular parasites use to exit from parasitophorous vacuoles and host cells, plays a very important role in the parasite life cycle and is central to Eimeria propagation and pathogenesis. Despite the importance of egress in the intracellular parasite's life cycle, very little information is known on this process compared to other steps, e.g., invasion. The present study was conducted to investigate the interplay between the host adaptive immune system and Eimeria egression. Splenic lymphocytes or soluble immune factors were incubated with parasite-infected host cells for 3 or 5 h, and the percentage of egress was calculated according to an established formula. Viability of egressed parasites and host cells was tested using trypan blue exclusion and annexin V and propidium iodide staining, respectively. We found that premature egression of sporozoites from Eimeria tenella-infected primary chicken kidney cells or from chicken peripheral blood mononuclear cells occurred when the cells were cocultured in vitro with spleen lymphocytes from E. tenella-infected chickens but not when they were cocultured with splenocytes from uninfected chickens. Eimeria-specific antibodies and cytokines (gamma interferon [IFN-␥], interleukin-2 [IL-2], and IL-15), derived from E. tenella-primed B and T lymphocytes, respectively, were capable of promoting premature egress of sporozoites from infected host cells. Both egressed parasites and host cells were viable, although the latter showed reduced reinvasion ability. These results suggest a novel, immune-mediated mechanism that the host exploits to interrupt the normal Eimeria life cycle in vivo and thereby block the release of mature parasites into the environment.

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Is Toxoplasma egress the first step in invasion?

Cited by 73 publications

References 34 publications

Molecular and functional aspects of parasite invasion

Molecular and functional aspects of parasite invasion

Evaluation of Five Antischizophrenic Agents Against Toxoplasma gondii in Human Cell Cultures

Enhanced Egress of Intracellular Eimeria tenella Sporozoites by Splenic Lymphocytes from Coccidian-Infected Chickens

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