ArticleJournal of immunology (Baltimore, Md. : 1950)2009
Externally triggered egress is the major fate of Toxoplasma gondii during acute infection.
Article in Journal of immunology (Baltimore, Md. : 1950), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
25 citing papers in PubMed.
- An in vivo fitness gene of Toxoplasma, MIC11, is essential for PLP1-mediated egress from host cells.Nature communications · 2026Article
- Article
- Effective factors in the pathogenesis ofHeliyon · 2024Review
- Egress Regulatory Factors: HowPathogens (Basel, Switzerland) · 2023Review
- Exogenous nitric oxide stimulates early egress of Eimeria tenella sporozoites from primary chicken kidney cells in vitro.Parasite (Paris, France) · 2021Article
- In Vivo CRISPR Screen Identifies TgWIP as a Toxoplasma Modulator of Dendritic Cell Migration.Cell host & microbe · 2019Article
- AmBio · 2019Article
- Phosphatidic acid governs natural egress in Toxoplasma gondii via a guanylate cyclase receptor platform.Nature microbiology · 2019Article
- Review
- Calcium signaling and the lytic cycle of the Apicomplexan parasite Toxoplasma gondii.Biochimica et biophysica acta. Molecular cell research · 2018Review
- A Window toPathogens (Basel, Switzerland) · 2018Review
- Exogenous tumor necrosis factor-alpha could induce egress of Toxoplasma gondii from human foreskin fibroblast cells.Parasite (Paris, France) · 2017Article
- The calcium signaling toolkit of the Apicomplexan parasites Toxoplasma gondii and Plasmodium spp.Cell calcium · 2015Review
- Ethanol and isopropanol trigger rapid egress of intracellular Eimeria tenella sporozoites.Parasitology research · 2015Article
- Lytic Cycle of Toxoplasma gondii: 15 Years Later.Annual review of microbiology · 2015Review
- Calcium entry in Toxoplasma gondii and its enhancing effect of invasion-linked traits.The Journal of biological chemistry · 2014Article
- Cell death of gamma interferon-stimulated human fibroblasts upon Toxoplasma gondii infection induces early parasite egress and limits parasite replication.Infection and immunity · 2013Article
- Prison break: pathogens' strategies to egress from host cells.Microbiology and molecular biology reviews : MMBR · 2012Review
- A genetic screen to isolate Toxoplasma gondii host-cell egress mutants.Journal of visualized experiments : JoVE · 2012Article
- A forward genetic screen reveals that calcium-dependent protein kinase 3 regulates egress in Toxoplasma.PLoS pathogens · 2012Article
Corrections and comments
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Authors and funding
4 authors.
Funding
Abstract
The apicomplexan parasite Toxoplasma gondii expands during acute infection via a cycle of invasion, intracellular replication, and lytic egress. Physiological regulation has not yet been demonstrated for either invasion or egress. We now report that, in contrast to cell culture systems, in which egress occurs only after five or more parasite divisions (2-3 days), intracellular residence is strikingly abbreviated in inflammatory cells in vivo, and early egress (after zero to two divisions) is the dominant parasite fate in acutely infected mice. Adoptive transfer experiments demonstrate rapid, reciprocal, kinetically uniform parasite transfer between donor and recipient compartments, with a t(1/2) of approximately 3 h. Inflammatory macrophages are major participants in this cycle of lytic egress and reinfection, which drives rapid macrophage turnover. Inflammatory triggering cells, principally macrophages, elicit egress in infected target macrophages, a process we term externally triggered egress (ETE). The mechanism of ETE does not require reactive oxygen or nitrogen species, the mitochondrial permeability transition pore, or a variety of signal transduction mediators, but is dependent on intracellular calcium and is highly sensitive to SB203580, an inhibitor of p38 MAPK as well as a related parasite-encoded kinase. SB203580 both inhibited the initiation of ETE and altered the progression of egress. Parasites recently completing a cycle of egress and reinfection were preferentially restricted in vivo, supporting a model in which ETE may favor host defense by a process of haven disruption. ETE represents a novel example of interaction between a parasite infectious cycle and host microenvironment.
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