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Abstract
Infection by the protozoan Toxoplasma gondii can have a devastating impact on the structure and function of the brain of the infected individuals, particularly immunocompromised patients. A systems biology view of the brain transcriptome can identify key molecular targets and pathways that mediate the neuropathogenesis of cerebral toxoplasmosis. Here, we performed transcriptomic analysis of the brain of mice infected by T. gondii Pru strain oocysts at 11 and 33 days post-infection (dpi) compared to uninfected (control) mice using RNA sequencing (RNA-seq). T. gondii altered the expression of 936 and 2,081 transcripts at 11 and 33 dpi, respectively, and most of these were upregulated in the infected brains. Gene Ontology (GO) enrichment and pathway analysis showed that immune response, such as interferon-gamma (IFN-γ) responsive genes were strongly affected at 11dpi. Likewise, differentially expressed transcripts (DETs) related to T cell activation, cytokine production and immune cell proliferation were significantly altered at 33 dpi. Host-parasite interactome analysis showed that some DETs were involved in immune signaling, metabolism, biosynthesis-related processes and interspecies interaction. These findings should increase knowledge of the mouse brain transcriptome and the changes in transcriptional regulation and downstream signaling pathways during acute and chronic T. gondii infections.
Highlights
Toxoplasma gondii is a widely prevalent intracellular apicomplexan protozoan parasite which chronically infects approximately one-third of the world’s population (Tenter et al, 2000)
Ten randomly selected transcripts were confirmed by qRT-PCR, and the results were consistent with those obtained by RNA sequencing (RNA-seq), supporting the validity of the obtained transcriptomic RNA-seq data (Supplementary Table 2)
We compared the transcriptome of brain tissues of BALB/C mice infected by oocysts of the type II T. gondii Pru strain with that of uninfected mice at 11 and 33 dpi using RNA-seq profiling
Summary
Toxoplasma gondii is a widely prevalent intracellular apicomplexan protozoan parasite which chronically infects approximately one-third of the world’s population (Tenter et al, 2000). Infection by T. gondii does not normally cause clinical illness in humans, individuals whose immune system is compromised can develop serious health problems. Chronic T. gondii infection can lead to neurological disorders, such as bipolar disease and schizophrenia (Elsheikha et al, 2016; Elsheikha and Zhu, 2016; Shiojiri et al, 2019). The dormant T. gondii cysts can reactivate and cause severe encephalitis, leading neurological manifestations and even fatal consequences (Wohlfert et al, 2017). T. gondii infections represent one of the major health challenges that compromise the life of people with HIV and remain a prominent cause of morbidity and mortalities in immunocompromised patients in general (Mayor et al, 2011). One study reported that 65% of HIV patients died within the first year of diagnosis with reactivated latent toxoplasmosis (Mayor et al, 2011)
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