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The CSF1R-Microglia Axis Has Protective Host-Specific Roles During Neurotropic Picornavirus Infection

ABSTRACT: The CSF1R-Microglia Axis Has Protective Host-Specific Roles During Neurotropic Picornavirus Infection

PROVIDER: PRJNA673884 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12966400.fastq.gz	Fastqsanger.gz
	SRR12966401.fastq.gz	Fastqsanger.gz
	SRR12966402.fastq.gz	Fastqsanger.gz
	SRR12966403.fastq.gz	Fastqsanger.gz
	SRR12966404.fastq.gz	Fastqsanger.gz

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The CSF1R-Microglia Axis Has Protective Host-Specific Roles During Neurotropic Picornavirus Infection

Project description:Goal: Determine the role of microglia in the antiviral response during neurotropic picornavirus infection of C57BL/6J and SJL/J mice and whether absence of microglia would affect CD4 and CD8 T cell functions. Methods: Brains from C57BL/6J and SJL/J mice treated with PLX5622 (to deplete microlgia) or control diet were harvested at 6 days post TMEV-infection. CD4+ T cells and CD8+ T cells were obtained using Easy Sep Mouse CD4+ T cell isolation Kit and Easy Sep Mouse CD8+ T cell isolation Kit (Stemcell). RNA was obtained using RNeasy (QIAGEN) and Illumina TruSeq stranded RNA Kit with Ribo-Zero Gold was then utilized to prepare cDNA library for RNA-seq. Results: Our results demonstrate strain-specific effects of the CSF1R-microglia axis in the context of neurotropic viral infection as well as inherent differences in microglial antigen presentation and subsequent T cell crosstalk that contribute to susceptibility to neurotropic picornavirus infection.

2021-05-10 | GSE160660 | GEO

The CSF1R-Microglia Axis Has Protective Host-Specific Roles During Neurotropic Picornavirus Infection.

Project description:Viral encephalitis is a major cause of morbidity and mortality, but the manifestation of disease varies greatly between individuals even in response to the same virus. Microglia are professional antigen presenting cells that reside in the central nervous system (CNS) parenchyma that are poised to respond to viral insults. However, the role of microglia in initiating and coordinating the antiviral response is not completely understood. Utilizing Theiler's murine encephalomyelitis virus (TMEV), a neurotropic picornavirus, and PLX5622, a small molecule inhibitor of colony-stimulating factor 1 receptor (CSF1R) signaling that can deplete microglia in the CNS; we investigated the role of the CSF1R-microglia axis in neurotropic picornavirus infection of C57BL/6J and SJL/J mice. These mouse strains differ in their ability to clear TMEV and exhibit different neurological disease in response to TMEV infection. CSF1R antagonism in C57BL/6J mice, which normally clear TMEV in the CNS, led to acute fatal encephalitis. In contrast, CSF1R antagonism in SJL/J mice, which normally develop a chronic CNS TMEV infection, did not result in acute encephalitis, but exacerbated TMEV-induced demyelination. Immunologically, inhibition of CSF1R in C57BL/6J mice reduced major histocompatibility complex II expression in microglia, decreased the proportion of regulatory T cells in the CNS, and upregulated proinflammatory pathways in CNS T cells. Acute CSF1R inhibition in SJL/J mice had no effect on microglial MHC-II expression and upregulated anti-inflammatory pathways in CNS T cells, however chronic CSF1R inhibition resulted in broad immunosuppression. Our results demonstrate strain-specific effects of the CSF1R-microglia axis in the context of neurotropic viral infection as well as inherent differences in microglial antigen presentation and subsequent T cell crosstalk that contribute to susceptibility to neurotropic picornavirus infection.

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Project description:iPSC-derived microglia expressing the wildtype, G795A, or G795C CSF1R variants were generated in vitro and treated with either DMSO or Plexxicon 5622 in order to compare the gene expression differences exising between genotypes at baseline or following CSF1R inhibtion.

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single-cell RNA-seq profile of adult microglia under acute Csf1r inhibition and early repopulation

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MAVS signaling shapes microglia responses to neurotropic virus infection

Project description:Viral encephalitis is characterized by a series of immunological reactions that can control virus infection in the brain, but dysregulated responses may cause excessive inflammation and brain damage. Microglia are brain-resident myeloid cells that are specialized on surveillance of the local environment and in case of viral brain infection they contribute to control of the infection and restriction of viral dissemination. Here, we report that after exposure to neurotropic vesicular stomatitis virus (VSV), murine in vitro microglia cultures showed rapid upregulation of a broad range of pro-inflammatory and antiviral genes, which were stably expressed over the entire 8 hours infection period. Additionally, a set of immunomodulatory genes was upregulated between 6 and 8 hours post infection. In in vitro microglia, the induction of several immune response pathways including cytokine responses was dependent on mitochondrial antiviral-signaling protein (MAVS). Consequently, in Mavs-deficient microglia control of virus infection failed as indicated by augmented accumulation of viral transcripts. Thus, in the analyzed in vitro system, MAVS signaling is critically required to achieve full microglia activation and to mediate profound antiviral effects. In Mavs-deficient mice, intranasal VSV instillation caused higher disease severity than in WT mice and the virus disseminated beyond the olfactory bulb and entered more distal brain regions. Virus spread to inner regions of the olfactory bulb, i.e., the granular cell layer, correlated with infiltration of highly inflammatory non-microglial myeloid cells into the olfactory bulb. Furthermore, increased cytokine levels were detected in the nasal cavity, the olfactory bulb and in other brain regions. Thus, microglial MAVS signaling is critically needed for virus sensing, full microglia activation, and for orchestration of protective immunity in the virus-infected CNS.

2024-08-29 | GSE274915 | GEO

Zebrafish control and csf1r mutant microglia transcriptomes

Project description:Purpose: Identify zebrafish control and csf1r-mutant microglia transcriptomes Methods: RNA sequencing was performed on FACS-sorted control microglia (3x), csf1ra-/- microglia (3x) and csf1ra-/-;b+/- microglia (3x). 10-20 million reads per sample were obtained. Reads were mapped to zebrafish genome GRC10. Results: We identified that csf1ra-/- or csf1ra-/-;b+/- microglia transcriptomes retain most of the microglia gene expression signature but mostly show changes in chemoklines expression.

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Zebrafish control and csf1r mutant microglia transcriptomes

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