ArticleInternational journal for parasitology2012
Host metabolism regulates growth and differentiation of Toxoplasma gondii.
Article in International journal for parasitology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
What it found
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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
22 citing papers in PubMed, 40 citations in OpenAlex.
- PI3K/Akt/mTOR signaling pathway mediates energy metabolic reprogramming and regulates mitochondrial homeostasis in host cells exposed toMicrobiology spectrum · 2026Article
- Exploring glycolytic enzymes in disease: potential biomarkers and therapeutic targets in neurodegeneration, cancer and parasitic infections.Open biology · 2025Review
- Article
- Constitutive upregulation of transcription factors underlies permissive bradyzoite differentiation in a natural isolate ofbioRxiv : the preprint server for biology · 2024Article
- Protein Lactylation and Metabolic Regulation of the Zoonotic Parasite Toxoplasma gondii.Genomics, proteomics & bioinformatics · 2023Article
- Tryptophan metabolism and immune alterations in pregnant Hispanic women with chronic Toxoplasma gondii infection.American journal of reproductive immunology (New York, N.Y. : 1989) · 2023Article
- Metabolic changes to host cells withbioRxiv : the preprint server for biology · 2023Article
- In vitro maturation of Toxoplasma gondii bradyzoites in human myotubes and their metabolomic characterization.Nature communications · 2022Article
- The determinants regulatingFrontiers in microbiology · 2022Review
- Biochemical Studies of Mitochondrial Malate: Quinone Oxidoreductase fromInternational journal of molecular sciences · 2021Article
- The Redox Homeostasis of Skeletal Muscle Cells Regulates Stage Differentiation ofFrontiers in cellular and infection microbiology · 2021Article
- Infection and Immunometabolism in the Central Nervous System: A Possible Mechanistic Link Between Metabolic Imbalance and Dementia.Frontiers in cellular neuroscience · 2021Review
- The Bradyzoite: A Key Developmental Stage for the Persistence and Pathogenesis of Toxoplasmosis.Pathogens (Basel, Switzerland) · 2020Review
- A latent ability to persist: differentiation in Toxoplasma gondii.Cellular and molecular life sciences : CMLS · 2018Review
- Toxoplasma gondii-positive human sera recognise intracellular tachyzoites and bradyzoites with diverse patterns of immunoreactivity.International journal for parasitology · 2018Article
- Metabolic interactions betweenF1000Research · 2018Review
- Toxoplasma gondii and Neospora caninum induce different host cell responses at proteome-wide phosphorylation events; a step forward for uncovering the biological differences between these closely related parasites.Parasitology research · 2017Article
- Impact of the host onMicrobial cell (Graz, Austria) · 2017Review
- Deletion of mitogen-activated protein kinase 1 inhibits development and growth of Toxoplasma gondii.Parasitology research · 2016Article
- Development of dual fluorescent stage specific reporter strain of Toxoplasma gondii to follow tachyzoite and bradyzoite development in vitro and in vivo.Microbes and infection · 2016Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
A critical step in the pathogenesis of Toxoplasma gondii is conversion from the fast-replicating tachyzoite form experienced during acute infection to the slow-replicating bradyzoite form that establishes long-lived tissue cysts during chronic infection. Bradyzoite cyst development exhibits a clear tissue tropism in vivo, yet conditions of the host cell environment that influence this tropism remain unclear. Using an in vitro assay of bradyzoite conversion, we have found that cell types differ dramatically in the ability to facilitate differentiation of tachyzoites into bradyzoites. Characterization of cell types that were either resistant or permissive for conversion revealed that resistant cell lines release low molecular weight metabolites that could support tachyzoite growth under metabolic stress conditions and thereby inhibit bradyzoite formation in permissive cells. Biochemical analysis revealed that the glycolytic metabolite lactate is an inhibitory component of supernatants from resistant cells. Furthermore, upregulation of glycolysis in permissive cells through the addition of glucose or by overexpression of the host kinase, Akt, was sufficient to convert cells from a permissive to a resistant phenotype. These results suggest that the metabolic state of the host cell may play a role in determining the predilection of the parasite to switch from the tachyzoite to bradyzoite form.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.