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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.

| S-EPMC8458822 | biostudies-literature

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Sparus aurata strain:picornavirus | isolate:QQ241

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scRNA-seq data of CSF1R WT/WT, naïve CSF1R WT/I792T and Mr BMT-treated CSF1R WT/I792T (deficient gene replaced by normal gene) mice brain cells.

Project description:To further characterize the influence of Mr BMT on the brains of ALSP mouse, we harvested brains from CSF1R WT/WT, naïve CSF1R WT/I792T and Mr BMT-treated CSF1R WT/I792T (deficient gene replaced by normal gene) mice for single-cell RNA-sequencing (scRNA-seq)

2025-07-12 | GSE270262 | GEO

RNA-SEQ of epithelioid mouse mesothelioma treated with or without CSF1R inhibitor

Project description:Mesothelioma arises in humans after prolonged chronic inflammation driven by the presence of inhaled asbestos fibres in the chest cavity. We have generated a genetically engineered mouse model of mesothelioma that combines CRE-mediated deletion of 3 disease-relevant tumour suppressor genes, namely Cdkn2a, Nf2 and p53, with a single intrapleural injection of asbestos. Tumours arising in these mice are heavily infiltrated by macrophages, which play. key roles in tumour development and are thought to create a permissive environment for tumour growth. We used a CSF1R inhibitor, AZD7507, to suppress macrophages, starting from day 60 post tumour initiation. This experiment analysed the overall tumour transcriptome in response to macrophage suppression

2023-06-03 | E-MTAB-12998 | biostudies-arrayexpress

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Project description:Genome characterization, prevalence and transmission mode of a novel picornavirus associated with the Threespine Stickleback (Gasterosteus aculeatus)

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Gene expression in spinal cord microglia during demyelination and remyelination following neuroattenuated JHMV infection

Project description:Microglia are considered both pathogenic and protective during recovery from demyelination, but their precise role remains ill-defined. Here, using an inhibitor of colony stimulating factor 1 receptor (CSF1R), PLX5622, and mice infected with a neurotropic coronavirus (mouse hepatitis virus, strain JHMV), we show that depletion of microglia after clearance of virus infection resulted in impaired myelin repair and prolonged clinical disease. Microglia were required only during the early stages of remyelination. Notably, large deposits of extracellular vesiculated myelin and cellular debris were detected in the spinal cords of PLX5622-treated and not control mice, which correlated with decreased numbers of oligodendrocytes in demyelinating lesions in drug-treated mice. Further, gene expression analyses demonstrated differential expression of genes involved in myelin debris clearance, lipid and cholesterol recycling, and promotion of oligodendrocyte function. The results also demonstrate that microglial function could not be compensated by infiltrating macrophages. Together, these results demonstrate key roles for microglia in debris clearance and the initiation of remyelination following infection with a neurotropic coronavirus but are not necessary during later stages of remyelination.

2020-02-07 | GSE144911 | GEO

Gene expression data of CSF1R antibody-treated myeloma-associated macrophages

Project description:Colony-stimulating factor 1 receptor (CSF1R) signaling controls MФ differentiation and function, and blocking CSF1R exerts antitumor effects in solid tumors. We examined the effects of CSF1R blockade on multiple therapy. Our results showed that CSF1R blockade inhibited the differentiation, proliferation and survival of M2 and myeloma-associated MФs (MAMs). Microarray was used for determining CS7 effect on polarization of MAMs. We used microarrays to detail the global programme of gene expression underlying polarizaiton of myeloma-associated macrophages by CSF1R antibody treatment and identified distinct classes of polarization-related genes during this process.

2017-06-30 | GSE99393 | GEO

Effect of CSF1R targeting on human macrophages in normoxia and hypoxia

Project description:CSF1R is a receptor involved in differentiation and survival of macrophages. We designed this study to explore the consequences of CSF1R targeting on human macrophage transcriptome. We also seek to explore the influence of oxygen environnment on the consequences of CSF1R blocakde . Our data provide an extensive characterization of the various pathways connected to CSF1/CSF1R pathway in human macrophages.

2024-04-18 | GSE263919 | GEO

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