miR-146a and miR-155 Delineate a MicroRNA Fingerprint Associated with Toxoplasma Persistence in the Host Brain

Cannella, Dominique; Brenier-Pinchart, Marie-Pierre; Braun, Laurence; Rooyen, Jason M. van; Bougdour, Alexandre; Bastien, Olivier; Behnke, Michael S.; Curt, Rose-Laurence; Curt, Aurélie; Saeij, Jeroen P. J.; Sibley, L. David; Pelloux, Hervé; Hakimi, Mohamed‐Ali

doi:10.1016/j.celrep.2014.02.002

Cited by 82 publications

(78 citation statements)

References 25 publications

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“…Perhaps one of the best characterized miRs involved in parasitic infection is miR‐155. This potent oncomiR is linked to tumorigenesis, inflammation and is induced by bacterial, viral and protozoan pathogens, including Helicobacter pylori , Epstein–Barr virus, Toxoplasma , Cryptosporidium and Theileria (Hakimi and Cannella, ; Marsolier et al ., ; Cannella et al ., ). Here again, Theileria provides a fascinating example supporting the epigenator‐initiator‐maintainer model by illustrating how miR‐155 acts as an epigenetic maintainer by generating an addictive feedback loop underlying the transformed phenotypes of infected cells (Marsolier et al ., ).…”

Section: Epigenetic Maintainers: Micro‐management and Feedback Loopsmentioning

confidence: 97%

Host–parasite interactions: an intimate epigenetic relationship

Cheeseman

Weitzman

2015

Cell Microbiol

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SummaryThe epigenetics of host-pathogen interactions is emerging as an interesting angle from which to study how parasites have evolved sophisticated strategies to manipulate host gene transcription and protein expression. In this review, we discuss the application of an operational framework to investigate the host cell signalling pathways that are induced by intracellular parasites and the epigenomic consequences in the host nucleus. To illustrate this conceptual approach, we have focused on examples from two eukaryotic intracellular parasites of the apicomplexa phylum: Theileria and Toxoplasma. We review recent findings on intracellular parasitism strategies for hijacking host nuclear functions and discuss how we might think of the parasite and its proteome as an intracellular epigenator.

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Section: Epigenetic Maintainers: Micro‐management and Feedback Loopsmentioning

confidence: 97%

Host–parasite interactions: an intimate epigenetic relationship

Cheeseman

Weitzman

2015

Cell Microbiol

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“…miRNAs are abundant in the nervous system and a link between miRNAs and the occurrence and development of neurological diseases, such as cerebral ischemia, stroke and neurodegenerative diseases, is becoming increasingly clear [15]. Notably, miRNAs are also found to be regulators of the host response to Toxoplasma infection, as miR-146a and miR-155 are highly induced in chronically infected mice brain, but worthy to mention, compared to miR-146a −/− mice, wild type mice show a more severe TE after challenge with genotype II Pru strain [16]. In addition to using host miRNAs for parasite persistence, T. gondii infection also modulates host cell miRNA profiles in a timely manner [17].…”

Section: Introductionmentioning

confidence: 99%

miRNA and circRNA expression patterns in mouse brain during toxoplasmosis development

Zhou

Huang

et al. 2020

BMC Genomics

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Background: 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. Results: Total 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. Conclusions: These 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.

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“…miRNAs function as important posttranscriptional regulators of gene expression by pairing with the 3′ untranslated regions of target genes, thereby inhibiting translation and/or promoting degradation of mRNA (18). miRNAs, including miR-155, have been shown to regulate host response to apicomplexan parasites such as Toxoplasma (19). Brain endothelial miR-155 is also reported to negatively regulate BBB function during neuroinflammation associated with experimental autoimmune encephalomyelitis (EAE), a model of multiple sclerosis (MS), and systemic inflammation induced by lipopolysaccharide (20).…”

Section: Introductionmentioning

confidence: 99%

miR-155 Modifies Inflammation, Endothelial Activation and Blood-Brain Barrier Dysfunction in Cerebral Malaria

Barker

Kim

et al. 2017

Mol Med

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miR-155 has been shown to participate in host response to infection and neuroinflammation via negative regulation of blood-brain barrier (BBB) integrity and T cell function. We hypothesized that miR-155 may contribute to the pathogenesis of cerebral malaria (CM). To test this hypothesis, we used a genetic approach to modulate miR-155 expression in an experimental model of cerebral malaria (ECM). In addition, an engineered endothelialized microvessel system and serum samples from Ugandan children with CM were used to examine anti-miR-155 as a potential adjunctive therapeutic for severe malaria. Despite higher parasitemia, survival was significantly improved in miR-155 -/-mice versus wild-type littermate mice in ECM. Improved survival was associated with preservation of BBB integrity and reduced endothelial activation, despite increased levels of proinflammatory cytokines. Pretreatment with antagomir-155 reduced vascular leak induced by human CM sera in an ex vivo endothelial microvessel model. These data provide evidence supporting a mechanistic role for miR-155 in host response to malaria via regulation of endothelial activation, microvascular leak and BBB dysfunction in CM.

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miR-146a and miR-155 Delineate a MicroRNA Fingerprint Associated with Toxoplasma Persistence in the Host Brain

Cited by 82 publications

References 25 publications

Host–parasite interactions: an intimate epigenetic relationship

Host–parasite interactions: an intimate epigenetic relationship

miRNA and circRNA expression patterns in mouse brain during toxoplasmosis development

miR-155 Modifies Inflammation, Endothelial Activation and Blood-Brain Barrier Dysfunction in Cerebral Malaria

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