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Serum neurofilament light reveals the contraction from widespread to lesion-bound neuroaxonal injury during autoimmune neuroinflammation

ABSTRACT: Serum neurofilament light reveals the contraction from widespread to lesion-bound neuroaxonal injury during autoimmune neuroinflammation

PROVIDER: PRJNA940750 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR23698535_1.fastq.gz	Fastqsanger.gz
	SRR23698535_2.fastq.gz	Fastqsanger.gz
	SRR23698536_1.fastq.gz	Fastqsanger.gz
	SRR23698536_2.fastq.gz	Fastqsanger.gz
	SRR23698537_1.fastq.gz	Fastqsanger.gz

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Serum neurofilament light reveals the contraction from widespread to lesion-bound neuroaxonal injury during autoimmune neuroinflammation

Project description:Blood-based neurofilament light (sNfL) indicates neuroaxonal injury in multiple sclerosis and is on the cusp of being implemented into clinical routine. However, anatomical origins and pathophysiological mechanisms of NfL release during acute relapses and later chronic disease stages are still poorly understood. Here, we applied immunohistochemistry, single molecule array, spatial transcriptomics and microglia/axon co-cultures to gain insight into spatio-temporal NfL release in experimental autoimmune encephalomyelitis (EAE). Results: Association of spinal cord white matter lesions and sNfL levels revealed a distinct, stage-dependent anatomical pattern of neuroaxonal damage: In chronic EAE, sNfL levels were predominately associated with anterolateral lumbar lesions, whereas in early EAE sNfL showed no correlation with lesions in any anatomical location. Furthermore, neuroaxonal damage in late EAE was largely confined to white matter lesions, but showed a widespread distribution in early EAE. Followingthis spatio-temporal pattern of neuroaxonal damage, spatial transcriptomics revealed a widespread cyto- and chemokine response at early disease stages, whereas late EAE was characterized by a prominent glial cell accumulation in white matter lesions. These findings were corroborated by immunohistochemistry and micro-glia/axon co-cultures, which further revealed a strong association between CNS myeloid cell activation and neuroaxonal damage both in vivo and in vitro. Interpretation: Our data demonstrate that sNfL release in EAE driven by CNS myeloid cells exhibits progress in a disease stage-dependent centripetal manner from normal-appearing white matter to focal white matter lesions. These findings may further aid the interpretation of elevated sNfL levels in multiple sclerosis patients at different disease stages.

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Project description:The present study had the purpose to analyze the transcriptional state of oligodendrocytes in an animal model of multiple scleroris resembling autoimmune neuroinflammation and compared with control mice treated with ovalbumin. The results revealed that oligodendrocytes from the EAE (experimental autoimmune encephalomyelitis) model upregulate genes that are involved in immune processes providing evidence that oligodendrocytes can develop an immune phenotype in particular neuroinflammatory conditions.

2021-08-21 | GSE182341 | GEO

Microglial expression of CD83 governs cellular activation and restrains autoimmune neuroinflammation

Project description:Microglial activation during neuroinflammation is crucial for coordinating the immune response against neuronal tissue and the initial response of microglia determines the severity of neuroinflammatory diseases. CD83 has been associated with early activation of microglia in various disease settings albeit its functional relevance for microglial biology was still elusive. Thus, we conducted a thorough assessment of CD83 regulation in microglia as well as its impact on microglial mediated neuroinflammation. Here, we describe for the first time that CD83 expression in microglia is not only associated with cellular activation but also with pro-resolving functions. Conditional deletion of CD83 causes malfunctioning responses to myelin debris, which results in an over-activated state during autoimmune neuroinflammation. Subsequently, CD83-deficient microglia recruit more pathogenic immune cells to the central nervous system and deteriorate resolving mechanism, which exacerbates the disease. Thus, CD83 in microglia orchestrates cellular activation and consequently, also resolution of neuroinflammation.

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2009-10-15 | E-GEOD-18136 | biostudies-arrayexpress

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Resident macrophage enhances an autoimmune lesion in Sjögren's syndrome

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Vagus Nerve Stimulation enhances remyelination and decreases innate neuroinflammation in a Multiple Sclerosis rodent model.

Project description:This study investigated the effect of Vagus Nerve Stimulation (VNS) on innate neuroinflammation and remyelination in lysolecithin (LPC) induced demyelination, a preclinical model for Multiple Sclerosis (MS). In a first experiment (demyelination experiment), LPC was injected in the corpus callosum of 33 Lewis rats, inducing a demyelinated lesion, and rats were treated with either continuously-cycled VNS (cVNS) or one-minute per day VNS (1minVNS) or sham VNS, from two days before the injection until three days post-injection (dpi), when they were killed for immunohistochemistry and proteomics analysis. This timepoint corresponded with a demyelinated lesion and peak inflammation. In a second experiment (remyelination experiment), 13 rats were analogously treated with either cVNS or sham from two days before LPC injection until 11 dpi, when they were killed for tissue prelevation for immunohistochemistry and proteomics. This timepoints corresponded with partial remyelination of the lesion. For proteomics analysis, 20 rats were randomly selected, namely five cVNS and five sham rats of the demyelination experiment, and five cVNS and five sham rats of the remyelination experiment.

2024-05-10 | PXD050858 | Pride

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