Project description:Toxoplasma gondii is a protozoan parasite with a remarkable neurotropic affinity. We recently showed that T. gondii infection can alter the global metabolism of the cerebral cortex of the mice. However, the impact of this infection on the metabolism of the cerebellum remained unclear. In this study, we compared the metabolomic profiles of mouse cerebellum following acute and chronic infection with T. gondii. Three-week-old female BALB/c mice (n = 36) were commercially obtained from Lanzhou University Laboratory Animal Center (Lanzhou, China). Mice were separated into 6 groups (6 mice/group). The mice in the infected groups were challenged with 10 T. gondii cysts of PRU strain suspended in 0.5 ml phosphate-buffered saline (PBS), whereas the mice in the control groups were sham treated with 0.5 ml PBS only. All mice were provided non-medicated feed and water ad libitum during the experiment. The mice were monitored twice daily for signs of illness and mortality. At 7, 14, and 21 days post infection (dpi), mice from infected and control group were humanely sacrificed by CO2 asphyxiation and cerebellum of each mouse was dissected with scissors and forceps. Then, the metabolite profile changes in the cerebellum of mice following infection of T. gondii was analyzed.
Project description:This study is part of the immgenT Open Source Project, specifically IGT59, which characterizes activated CD4 and CD8 T cells in the spleen and brain during Toxoplasma gondii infection at 9 dpi (peak infection in the spleen) and 23 dpi (chronic phase with brain cysts). Splenocytes from uninfected controls were also profiled. It includes a spleen control at baseline (6-8-week-old C57BL/6J mouse).
Project description:This study is part of the immgenT Open Source Project, specifically IGT59, which characterizes activated CD4 and CD8 T cells in the spleen and brain during Toxoplasma gondii infection at 9 dpi (peak infection in the spleen) and 23 dpi (chronic phase with brain cysts). Splenocytes from uninfected controls were also profiled. It includes a spleen control at baseline (6-8-week-old C57BL/6J mouse).
Project description:The goal of this study was to identify the neural systems that underlie the behavorial changes in intermediate hosts of Toxoplasma gondii. Using a mouse whole genome microarray, we analyzed gene expression in the frontal cortex during the latent stages of infection. We found marked sex-dependent effects on gene transcription in mice. In female mice, Toxoplasma infection altered the expression of genes involved in the development of the forebrain, neurogenesis, sensory and motor coordination. In male mice, infection led mainly to modulation of genes associated with olfaction. Our results indicate that the gender of the host plays a major role in determining variable brain changes following Toxoplasma infection.
Project description:C57BL/6J mice were infected intraperitoneally with 20 cysts of Toxoplasma gondii. Peritoneal exudate cells were harvested on day 5 post-infection and profiled by single-cell CITE-seq (10x Genomics) using the BioLegend TotalSeq-B Mouse Universal Cocktail v1.0 to jointly measure transcriptome and cell-surface protein expression. This dataset was used to characterize T-bet (Tbx21) expression across myeloid populations during acute toxoplasmosis.
Project description:Toxoplasma gondii is a protozoan parasite with a remarkable neuro-tropismneurotropic affinity. We recently showed that T. gondii infection can alter the global metabolism of the cerebral cortex of the mice. However, the impact of this infection on the metabolism of the hippocampus remains unclear. In this study, we compared the metabolomic profiles of mouse hippocampus following acute and chronic infection with T. gondii. Our data provide new insight into the neuropathogenesis of T. gondii infection and reveal new pathways and metabolites that mediate the interplay between T. gondii infection and the mouse hippocampus
Project description:Toxoplasma gondii is a zoonotic pathogen for which felids serve as definitive hosts. In cats, the parasite undergoes several rounds of asexual replication before entering the sexual cycle which gives rise to oocysts that are shed into the environment. These then sporulate and become infective to humans and live stock. To understand the genes involved in the parasite development in the felid host and identify potential intervention targets, we designed a transcriptomic approach to compare the cat intestinal stages with the well characterised tachyzoites that mediate acute infection and tissue cysts that are responsible for chronic infection. Cats were infected with T. gondii tissue cysts from mouse brain and sampled the intestinal stages at day 3, 5 and 7 post infection. As an input sample, we also collected tissue cysts from mouse brain as well as in vitro cultivated tachyzoites. Total RNA was extracted, enriched for mRNA and used for cDNA synthesis. RNA-Seq was then performed to describe the transcriptomic repertoire of each time point/life cycle stage.
Project description:Timecourse following infection of the RAW264.7 murine macrophage cell line with Toxoplasma gondii, or mock infected, or stimulated with lysed Toxoplasma.