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ABSTRACT: Dimethyl itaconate ameliorates goal-directed behavior in Toxoplasma gondii infected mice

PROVIDER: PRJNA801463 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17994030_1.fastq.gz	Fastqsanger.gz
	SRR17994030_2.fastq.gz	Fastqsanger.gz
	SRR17994031_1.fastq.gz	Fastqsanger.gz
	SRR17994031_2.fastq.gz	Fastqsanger.gz
	SRR17994032_1.fastq.gz	Fastqsanger.gz

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The Sex-Specific Changes in Gene Expression and Behavior Induced by Chronic Toxoplasma Infection in Mice

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. Male and female BALB/c mice (infected female: n=5; infected male: n=5; female control: n=5; male control: n=4) were used in this study. They were sacrificed approximately 6 month post infection and the frontal cortices harvested. RNA transcript levels were quantified by microarray analyses using Illumina Mouse Ref-8 v2.0 Expression BeadChips.

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Project description:The closely related protozoan parasites Toxoplasma gondii and Neospora caninum display similar life cycles, subcellular ultrastructure, invasion mechanisms, metabolic pathways, and genome organization, but differ in their host range and disease pathogenesis. Type II (?) interferon has long been known to be the major mediator of innate and adaptive immunity to Toxoplasma infection, but genome-wide expression profiling of infected host cells indicates that Neospora is a potent activator of the type I (?/?) interferon pathways typically associated with antiviral responses. Infection of macrophages from mice with targeted deletions in various innate sensing genes demonstrates that host responses to Neospora are dependent on the toll-like receptor Tlr3 and the adapter protein Trif. Consistent with this observation, RNA from Neospora elicits type I interferon responses when targeted to the host endo-lysosomal system. While live Toxoplasma fails to induce type I interferon, heat-killed parasites do trigger this response, and co-infection studies reveal that T. gondii actively suppresses the production of type I interferon. These findings reveal that eukaryotic pathogens can be potent inducers of type I interferon and that some parasite species, like Toxoplasma gondii, have evolved mechanisms to suppress this response. In vitro cultures of bone marrow-derived macrophages from WT or IFNAR2-/- mice were infected with either Toxoplasma gondii (VEG strain) or Neospora caninum (Nc2 strain) for 17 hours. RNA was collected from biological replicates for expression profiling by microarray. Uninfected controls for both WT and IFNAR2-/- were used as a reference.

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