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Early Involvement of Peripherally Derived Monocytes in Inflammation in an NMO-Like Mouse Model [microglia]

ABSTRACT: Early Involvement of Peripherally Derived Monocytes in Inflammation in an NMO-Like Mouse Model [microglia]

PROVIDER: PRJNA985645 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24975232.fastq.gz	Fastqsanger.gz
	SRR24975233.fastq.gz	Fastqsanger.gz
	SRR24975234.fastq.gz	Fastqsanger.gz
	SRR24975235.fastq.gz	Fastqsanger.gz
	SRR24975236.fastq.gz	Fastqsanger.gz

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Similar Datasets

Early Involvement of Peripherally Derived Monocytes in Inflammation in an NMO-Like Mouse Model [microglia]

Project description:Neuromyelitis optica (NMO) is an autoimmune inflammatory disease that primarily affects the spinal cord and optic nerves in the central nervous system (CNS). It is characterized by the presence of immunoglobulin G (IgG) antibodies against aquaporin 4, a protein found in astrocytes (known as NMO-IgG). Monocytes/macrophages and microglia accumulate at the active injury sites and contribute to the disease process. However, it is unclear whether these active cells originate from circulating monocytes/macrophages or resident microglia. Recent studies have investigated the role of microglia/macrophages in multiple sclerosis (MS) using specific microglial markers, such as P2ry12 and Tmem119, and have shown that active cells are derived from microglia. In contrast, the function of monocyte/macrophages and microglia in NMO has not been extensively studied. Therefore, this study aims to analyze the functions of monocytes/macrophages and microglia using microglial markers (P2ry12 and Tmem119) in an NMO-like mouse model and evaluate their role in the pathophysiology of NMO.

2024-01-17 | GSE235276 | GEO

Early Involvement of Peripherally Derived Monocytes in Inflammation in an NMO-Like Mouse Model [Monocytes]

2024-01-17 | GSE235277 | GEO

Early Involvement of Peripherally Derived Monocytes in Inflammation in an NMO-Like Mouse Model [Monocytes]

Project description:Early Involvement of Peripherally Derived Monocytes in Inflammation in an NMO-Like Mouse Model [Monocytes]

| PRJNA985646 | ENA

Early Involvement of Peripherally Derived Monocytes in Inflammation in an NMO-Like Mouse Model

Project description:Early Involvement of Peripherally Derived Monocytes in Inflammation in an NMO-Like Mouse Model

| PRJNA985638 | ENA

Early involvement of peripherally derived monocytes in inflammation in an NMO-like mouse model.

Project description:Neuromyelitis optica (NMO) is an autoimmune inflammatory disease that primarily affects the optic nerve and spinal cord within the central nervous system (CNS). Acute astrocyte injury caused by autoantibodies against aquaporin 4 (NMO-IgG) is a well-established key factor in the pathogenesis, ultimately leading to neuronal damage and patient disability. In addition to these humoral immune processes, numerous innate immune cells were found in the acute lesions of NMO patients. However, the origin and function of these innate immune cells remain unclear in NMO pathogenesis. Therefore, this study aims to analyze the origin and functions of these innate immune cells in an NMO-like mouse model and evaluate their role in the pathophysiology of NMO. The expression of Tmem119 on Iba1 + cells in brain tissue disappeared immediately after the injection of NMO-IgG + human complement mixture, while the expression of P2ry12 remained well-maintained at 1 day after injection. Based on these observations, it was demonstrated that monocytes infiltrate the brain during the early stages of the pathological process and are closely associated with the inflammatory response through the expression of the proinflammatory cytokine IL-1β. Understanding the variations in the expression patterns of P2ry12, Tmem119, and other markers could be helpful in distinguishing between these cell types and further analyzing their functions. Therefore, this research may contribute to a better understanding of the mechanisms and potential treatments for NMO.

| S-EPMC10786844 | biostudies-literature

Early Involvement of Peripherally Derived Monocytes in Inflammation in an NMO-Like Mouse Model

Project description:This SuperSeries is composed of the SubSeries listed below.

2024-01-17 | GSE235278 | GEO

Gene expression signature of Lewis rats with experimental NMO and controls

Project description:study was performed to reveal the extent to which NMO-IgG contributes to tissue damage in experimental NMO Gene expression was studied in Lewis rats after transfer of myelin basic protein-specific T cells on day 0 and NMO-IgG on day 4. The animals were sacrificed 24 hours later. Controls did either not receive T cells (0), did receive control IgG or PBS instead of NMO-IgG, or were left completely untreated.

2016-03-22 | E-GEOD-73411 | biostudies-arrayexpress

Gene expression signature of Lewis rats with experimental NMO and controls

Project description:study was performed to reveal the extent to which NMO-IgG contributes to tissue damage in experimental NMO

2016-03-22 | GSE73411 | GEO

hUC-MSCs-derived MFGE8 ameliorates locomotor dysfunction via inhibition of ITGB3/NF-κB signaling in an NMO mouse model

Project description:Neuromyelitis optica (NMO) is a severe autoimmune inflammatory disease of the central nervous system that affects motor function and causes relapsing disability. Human umbilical cord-derived mesenchymal stem cells (hUC-MSCs) have been used extensively in the treatment of various inflammatory diseases, due to their potent regulatory roles that can mitigate inflammation and repair damaged tissues. However, their use in NMO is currently limited, and the mechanism underlying the beneficial effects of hUC-MSCs on motor function in NMO remains unclear. In this study, we investigate the effects of hUC-MSCs on the recovery of motor function in an NMO systemic model. Our findings demonstrate that milk fat globule epidermal growth 8 (MFGE8), a key functional factor secreted by hUC-MSCs, plays a critical role in ameliorating motor impairments. We also elucidate that the MFGE8/Integrin αvβ3/NF-κB signaling pathway is partially responsible for structural and functional recovery, in addition to motor functional enhancements induced by hUC-MSC exposure. Taken together, these findings strongly support the involvement of MFGE8 in mediating hUC-MSCs-induced improvements in motor functional recovery in an NMO mouse model. In addition, this provides new insight on the therapeutic potential of hUC-MSCs and the mechanisms underlying their beneficial effects in NMO.

2023-11-03 | GSE246608 | GEO

Peripherally derived macrophages can engraft the brain independent of irradiation and maintain an identity distinct from microglia

Project description:Peripherally derived macrophages infiltrate the brain after bone marrow transplantation and during central nervous system (CNS) inflammation. It was initially suggested that these engrafting cells were newly derived microglia and that irradiation was essential for engraftment to occur. However, it remains unclear whether brain-engrafting macrophages (beMφs) acquire a unique phenotype in the brain, whether long-term engraftment may occur without irradiation, and whether brain function is affected by the engrafted cells. In this study, we demonstrate that chronic, partial microglia depletion is sufficient for beMφs to populate the niche and that the presence of beMφs does not alter behavior. Furthermore, beMφs maintain a unique functional and transcriptional identity as compared with microglia. Overall, this study establishes beMφs as a unique CNS cell type and demonstrates that therapeutic engraftment of beMφs may be possible with irradiation-free conditioning regimens.

2018-04-07 | GSE84819 | GEO

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