ArticleThe Korean journal of parasitology2020
The Role of PI3K/AKT Pathway and NADPH Oxidase 4 in Host ROS Manipulation by Toxoplasma gondii.
Article in The Korean journal of parasitology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 9 citations in OpenAlex.
- β-catenin-driven innate and metabolic reprograming in macrophages fuel T-cell-dependent inflammation in Toxoplasma gondii infection: implications for therapeutic intervention.Cell death & disease · 2026Article
- Ferroptosis modulation by Toxoplasma gondii suppresses sodium iodate-driven age-related macular degeneration.Genes & genomics · 2026Article
- Parasites as Modulators of Angiogenesis: Implications for Vascular Biology and Pathogenesis.Pathogens (Basel, Switzerland) · 2026Review
- Small molecule kinase inhibitor altiratinib inhibits brain cyst forming bradyzoites of Toxoplasma gondii.Journal of microbiology (Seoul, Korea) · 2025Article
- Brain -cyst-driven genes expression in Toxoplasma Gondii Tehran strain: a parasitic-immunogenicity assessment by dint of RNA-Seq.Veterinary research communications · 2024Article
- Review
- Article
- Regulation of phosphoinositide metabolism in Apicomplexan parasites.Frontiers in cell and developmental biology · 2023Review
- FAF1 downregulation by Toxoplasma gondii enables host IRF3 mobilization and promotes parasite growth.Journal of cellular and molecular medicine · 2021Article
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Authors and funding
7 authors at 1 institution in 2 countries.
Funding
Abstract
Dendritic cell is one of the first innate immune cell to encounter T. gondii after the parasite crosses the host intestinal epithelium. T. gondii requires intact DC as a carrier to infiltrate into host central nervous system (CNS) without being detected or eliminated by host defense system. The mechanism by which T. gondii avoids innate immune defense of host cell, especially in the dendritic cell is unknown. Therefore, we examined the role of host PI3K/AKT signaling pathway activation by T. gondii in dendritic cell. T. gondii infection or T. gondii excretory/secretory antigen (TgESA) treatment to the murine dendritic cell line DC2.4 induced AKT phosphorylation, and treatment of PI3K inhibitors effectively suppressed the T. gondii proliferation but had no effect on infection rate or invasion rate. Furthermore, it is found that T. gondii or TgESA can reduce H2O2-induced intracellular reactive oxygen species (ROS) as well as host endogenous ROS via PI3K/AKT pathway activation. While searching for the main source of the ROS, we found that NADPH oxidase 4 (NOX4) expression was controlled by T. gondii infection or TgESA treatment, which is in correlation with previous observation of the ROS reduction by identical treatments. These findings suggest that the manipulation of the host PI3K/AKT signaling pathway and NOX4 expression is an essential mechanism for the down-regulation of ROS, and therefore, for the survival and the proliferation of T. gondii.
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