ArticleParasites & vectors2025
Toxoplasma gondii-induced host's high secretion of 25-hydroxycholesterol for immunoprotection.
Article in Parasites & vectors, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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
1 citing paper in PubMed.
- Lipidomic Profiling of Colonic Contents in Mice with AcuteMicroorganisms · 2026Article
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6 authors.
Funding
Abstract
backgroundToxoplasma gondii, a parasitic protozoan affecting approximately one-third of global population, causes opportunistic toxoplasmosis. It penetrates barriers to immune-privileged sites, causing encephalitis, retinochoroiditis, and fetal damage. The infection may be linked to neurodegenerative and psychiatric disorders. The T. gondii-host interaction mechanism remains central to understanding its pathogenesis. The changes in small molecule metabolites after infection, which affects the central nervous system (CNS) normal function, have been poorly characterized.
methodsThe metabolic alterations in brain tissues of sv129 mice infected by T. gondii at 9 days post-infection (DPI) were analyzed through untargeted metabolomic detection. Cholesterol metabolic reprogramming was assessed through analysis of related gene's transcription with quantitative reverse transcription polymerase chain reaction (qRT-PCR). The primary target cells responsible for cholesterol metabolic dysregulation were identified through detection of the secreted cytokines with enzyme-linked immunosorbent assay (ELISA). The T. gondii replication in host cells treated with 25-HC was evaluated using immunofluorescence assay (IFA). Transcriptomic analysis was performed to identify the differentially expressed genes (DEGs) in the host cells infected by T. gondii and/or treated with 25-HC, and the host cell M1 polarization was confirmed by qRT-PCR.
resultsBrain metabolomic profiling identified 19 differentially expressed metabolites (including 25-HC), primarily involved in amino acid metabolism and cholesterol metabolism pathways (biosynthesis of primary bile acids and steroids). Toxoplasma gondii infection triggered host cholesterol metabolic reprogramming and promoted 25-HC secretion from glial cells, which indirectly inhibited T. gondii's proliferation in host cells. Transcriptomic analysis revealed that 25-HC upregulated the expression of chemokines, C-type lectin receptors, and inflammation-related genes. Notably, 25-HC was verified to confer host resistance against T. gondii infection by promoting microglial M1 polarization.
conclusionsOur study demonstrated that T. gondii infection activates the CH25H-25-HC axis to induce microglial M1 polarization and cytokine secretion, thereby establishing an anti-Toxoplasma defense. These findings highlight the central role of cholesterol metabolism in T. gondii pathogenesis and provide innovative strategies for the diagnosis, prevention, and treatment of toxoplasmosis.
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