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Immunological role of platelets in Theiler’s virus-induced inflammatory demyelinating disease and myocarditis

ABSTRACT: Immunological role of platelets in Theiler’s virus-induced inflammatory demyelinating disease and myocarditis

PROVIDER: PRJNA1065441 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27574316_1.fastq.gz	Fastqsanger.gz
	SRR27574316_2.fastq.gz	Fastqsanger.gz
	SRR27574317_1.fastq.gz	Fastqsanger.gz
	SRR27574317_2.fastq.gz	Fastqsanger.gz
	SRR27574318_1.fastq.gz	Fastqsanger.gz

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Immunological role of platelets in Theiler’s virus-induced inflammatory demyelinating disease and myocarditis

Project description:Platelets have been immunologically associated with viral and immune-mediated diseases such as Severe acute respiratory syndrome coronavirus 2 (SARS‑CoV‑2) and Experimental autoim-mune encephalomyelitis (EAE). However, the role of platelets in Theiler’s murine encephalo-myelitis virus (TMEV)-induced myocarditis and inflammatory demyelination disease (IDD) is still unknown. We determine whether platelets were associated with TMEV infection and whether glycoprotein Ib alpha chain (GPIbα/CD42b) antibody injection could affect the pathogenicity of TMEV-induced myocarditis and TMEV-IDD. We conducted a mechanistic experiment by injecting TMEV-infected mice with the anti-GPIbα antibodies 0 and 5 days p.i. (“Early” group) or 18 and 22 days p.i. (“Late” group). Using in silico and in vivo approaches, we found platelets and platelet-related genes were associated with TMEV infection. Platelet depletion in Early and Late mice reduced fibrotic area in the heart, inflammatory demyelinating lesions with lower viral persistence in the CNS and altered antiviral antibody responses. Thus, platelets contribute to the pathogenesis of TMEV infection by promoting fibrosis and CNS inflammation. Platelet-depletion treatment might open new therapeutic approaches for TMEV-induced myocarditis and TMEV-IDD.

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The role of inflammatory macrophages in pathophysiology of experimental autoimmune myocarditis

Project description:Myocarditis is an inflammatory disease of the cardiac muscle characterized by an influx of inflammatory cells, predominantly of myeloid lineage. The progression of myocarditis to a dilated cardiomyopathy phenotype and heart failure is markedly influenced by TGF-β signalling. The aim of this study was to investigate the role of TGF-β signalling in inflammatory cardiac macrophages in the development of myocarditis and post-inflammatory fibrosis. Experimental autoimmune myocarditis (EAM) was induced in the LysM-Cre x R26-stop-EYFP x Tgfbr2-fl/fl transgenic mice showing impaired TGF-β signalling in the myeloid lineage and the LysM-Cre x R26-stop-EYFP control mice. Inflammatory macrophages were sorted from the inflamed hearts and analyzed for differential gene expression using whole genome transcriptomics.

2024-06-20 | GSE262658 | GEO

Exploring the Role of Platelets in Virus-Induced Inflammatory Demyelinating Disease and Myocarditis.

Project description:Theiler's murine encephalomyelitis virus (TMEV) infection has been used as a mouse model for two virus-induced organ-specific immune-mediated diseases. TMEV-induced demyelinating disease (TMEV-IDD) in the central nervous system (CNS) is a chronic inflammatory disease with viral persistence and an animal model of multiple sclerosis (MS) in humans. TMEV infection can also cause acute myocarditis with viral replication and immune cell infiltration in the heart, leading to cardiac fibrosis. Since platelets have been reported to modulate immune responses, we aimed to determine the role of platelets in TMEV infection. In transcriptome analyses of platelets, distinct sets of immune-related genes, including major histocompatibility complex (MHC) class I, were up- or downregulated in TMEV-infected mice at different time points. We depleted platelets from TMEV-infected mice by injecting them with platelet-specific antibodies. The platelet-depleted mice had significantly fewer viral antigen-positive cells in the CNS. Platelet depletion reduced the severities of TMEV-IDD and myocarditis, although the pathology scores did not reach statistical significance. Immunologically, the platelet-depleted mice had an increase in interferon (IFN)-γ production with a higher anti-TMEV IgG2a/IgG1 ratio. Thus, platelets may play roles in TMEV infection, such as gene expression, viral clearance, and anti-viral antibody isotype responses.

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Single-cell RNA-sequencing for dissecting the immunological network in autoimmune myocarditis

Project description:We report the scRNA-seq for cardiac immune cells in the different phases of experimental autoimmune myocarditis (EAM).

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Single-cell RNA-sequencing for dissecting the immunological network in autoimmune myocarditis

Project description:Single-cell RNA-sequencing for dissecting the immunological network in autoimmune myocarditis

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Pro-inflammatory activity following demyelinating injury is required for phagocytic function and oligodendrocyte formation

Project description:Remyelination can occur naturally in demyelinating lesions, but often fails in human demyelinating diseases such as multiple sclerosis (MS). The function of the innate immune system is essential for the regenerative response, but how exactly microglia and macrophages clear myelin debris after injury and tailor a specific regenerative response is unclear. Here, we asked whether pro-inflammatory microglial/macrophage activation is required for this process. We established a novel toxin-based spinal cord model of de- and remyelination in zebrafish and showed that pro-inflammatory nuclear factor κB (NF-κB) dependent activation occurs in phagocytes rapidly after myelin injury. We found that the pro-inflammatory response depends on myeloid differentiation primary response 88 (MyD88), the canonical adaptor for inflammatory signaling pathways downstream of toll-like receptors (TLRs). MyD88-deficient mice and zebrafish were impaired not only in the degradation of myelin debris, but also in initiating the generation of new oligodendrocytes for myelin repair. We identified reduced generation of tumor necrosis factor-α (TNF-α) in lesions of MyD88-deficient animals, a pro-inflammatory molecule that was able to induce the generation of new oligodendrocytes. Our study shows that pro-inflammatory phagocytic signaling is an evolutionary conserved mechanism necessary for degrading myelin debris, essential for inflammation resolution, and for initiating the secretion of pro-inflammatory myelin repair molecules.

2020-02-17 | PXD014625 | Pride

Sex differences during acute myocarditis against coxsackievirus B3 (CVB3)-induced myocarditis (10 dpi) and chronic myocarditis/dilated cardiomyopathy (DCM) against CVB3-induced myocarditis (90 dpi)

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Expression profiles of non-coding RNAs in the heart of mice with coxsackie B3 virus-induced myocarditis

Project description:Non-coding RNAs (ncRNAs) are critical regulators of viral infection and inflammatory responses. However, the roles of ncRNAs in acute myocarditis (AM)M) remain unclear.To identify ncRNAs involved in viral myocarditis pathogenesis by RNA-seq.

2021-08-16 | E-MTAB-10823 | biostudies-arrayexpress

Plasma exosomal miRNA profiles in pediatric fulminant myocarditis patients and healthy controls

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Sex differences during acute myocarditis against coxsackievirus B3 (CVB3)-induced myocarditis (10 dpi) and chronic myocarditis/dilated cardiomyopathy (DCM) against CVB3-induced myocarditis (90 dpi)

Project description:Men are at an increased risk of dying from heart failure caused by inflammatory heart diseases such as atherosclerosis, myocarditis and dilated cardiomyopathy (DCM). We previously showed that immune responses in the heart are phenotypically distinct in male compared to female mice 10 days after infection resulting in severe DCM in males. Groups consisted of Infected Males, Infected Females, Uninfected Males and Uninfected females. There are 3 mice per group. A total of 12 samples were analyzed in this experiment (12 for 10 dpi and 12 for 90 dpi).

2012-01-19 | E-GEOD-35182 | biostudies-arrayexpress

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