Abstract
BackgroundIncreasing evidence has shown that circular RNAs (circRNAs) are involved in neurodegenerative disorders, but their roles in neurological toxoplasmosis are yet to know. This study examined miRNA and circRNA expressions in mouse brain following oral infection with T. gondii Pru strain.ResultsTotal RNA extracted from acutely infected (11 days post infection (DPI)), chronically infected (35 DPI) and uninfected mouse brain samples were subjected to genome-wide small RNA sequencing. In the acutely infected mice, 9 circRNAs and 20 miRNAs were upregulated, whereas 67 circRNAs and 28 miRNAs were downregulated. In the chronically infected mice, 2 circRNAs and 42 miRNAs were upregulated, whereas 1 circRNA and 29 miRNAs were downregulated. Gene ontology analysis predicted that the host genes that produced the dysregulated circRNAs in the acutely infected brain were primarily involved in response to stimulus and ion binding activities. Furthermore, predictive interaction networks of circRNA-miRNA and miRNA-mRNA were constructed based on genome-wide transcriptome sequencing and computational analyses, which might suggest the putative functions of miRNAs and circRNAs as a large class of post-transcriptional regulators.ConclusionsThese findings will shed light on circRNA-miRNA interactions during the pathogenesis of toxoplasmosis, and they will lay solid foundation for studying the potential regulation roles of miRNAs and circRNAs in T. gondii induced pathogenesis.
Highlights
Increasing evidence has shown that circular RNAs are involved in neurodegenerative disorders, but their roles in neurological toxoplasmosis are yet to know
The mapped reads were divided into different categories, and the majority of small RNA reads were belonged to the annotated known miRNAs
Using RNA-seq data, we revealed a global bias for miRNA and circular RNA (circRNA) accumulation in T. gondii infected mouse brains
Summary
Increasing evidence has shown that circular RNAs (circRNAs) are involved in neurodegenerative disorders, but their roles in neurological toxoplasmosis are yet to know. This study examined miRNA and circRNA expressions in mouse brain following oral infection with T. gondii Pru strain. Toxoplasma gondii, the causative agent of toxoplasmosis, is a medically important parasite infecting approximately 30% of the world’s population [1]. Immune-potent individuals usually do not show any clinical symptoms, and infection is latent and maintained inside the host as tissue cysts. When infected persons become immunocompromised, such as people suffering from AIDS or organ transplantation, parasite cyst reactivation can lead to acute toxoplasmosis, which includes eye disease, The fast proliferating T. gondii tachyzoite is fully controlled by the host potent immune response and transforms into a slowly replicating stage (i.e. bradyzoite) enclosed in tissue cysts, and remains dormant within the central nervous system (CNS) and muscles [4]. It has been shown that T. gondii infection can affect levels
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