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Pro-inflammatory monocyte phenotype during acute progression of cerebral small vessel disease

ABSTRACT: Pro-inflammatory monocyte phenotype during acute progression of cerebral small vessel disease

PROVIDER: PRJNA683025 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13208439.fastq.gz	Fastqsanger.gz
	SRR13208440.fastq.gz	Fastqsanger.gz
	SRR13208441.fastq.gz	Fastqsanger.gz
	SRR13208442.fastq.gz	Fastqsanger.gz
	SRR13208443.fastq.gz	Fastqsanger.gz

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Pro-inflammatory monocyte phenotype during acute progression of cerebral small vessel disease

Project description:The aetiology of cerebral small vessel disease (SVD) remains elusive, though currently evidence is accumulating that inflammation contributes to its pathophysiology. In this prospective high-frequency imaging study, we showed that the incidence of acute SVD progression coincides with a functional and transcriptional pro-inflammatory monocyte phenotype. To detect SVD progression, individuals with SVD underwent monthly magnetic resonance imaging (MRI) for 10 consecutive months. RNA sequencing revealed a pro-inflammatory monocyte signature with upregulation of the EGR2 gene. Collectively, we showed that individuals with progressive SVD have pro-inflammatory circulating monocytes characterized by an augmented cytokine production capacity and a pro-inflammatory transcriptional signature.

2020-12-09 | GSE162790 | GEO

Pro-inflammatory Monocyte Phenotype During Acute Progression of Cerebral Small Vessel Disease.

Project description:Background: The etiology of cerebral small vessel disease (SVD) remains elusive, though evidence is accumulating that inflammation contributes to its pathophysiology. We recently showed retrospectively that pro-inflammatory monocytes are associated with the long-term progression of white matter hyperintensities (WMHs). In this prospective high-frequency imaging study, we hypothesize that the incidence of SVD progression coincides with a pro-inflammatory monocyte phenotype. Methods: Individuals with SVD underwent monthly magnetic resonance imaging (MRI) for 10 consecutive months to detect SVD progression, defined as acute diffusion-weighted imaging-positive (DWI+) lesions, incident microbleeds, incident lacunes, and WMH progression. Circulating inflammatory markers were measured, cytokine production capacity of monocytes was assessed after ex vivo stimulation, and RNA sequencing was performed on isolated monocytes in a subset of participants. Results: 13 out of 35 individuals developed SVD progression (70 ± 6 years, 54% men) based on incident lesions (n = 7) and/or upper quartile WMH progression (n = 9). Circulating E-selectin concentration (p < 0.05) and the cytokine production capacity of interleukin (IL)-1β and IL-6 (p < 0.01) were higher in individuals with SVD progression. Moreover, RNA sequencing revealed a pro-inflammatory monocyte signature including genes involved in myelination, blood-brain barrier, and endothelial-leukocyte interaction. Conclusions: Circulating monocytes of individuals with progressive SVD have an inflammatory phenotype, characterized by an increased cytokine production capacity and a pro-inflammatory transcriptional signature.

| S-EPMC8155247 | biostudies-literature

Cerebrovascular p16INK4A expression induces cerebral small vessel disease-related phenotypes

Project description:Cerebrovascular p16INK4A expression induces cerebral small vessel disease-related phenotypes

| PRJNA1302351 | ENA

Cerebrovascular p16INK4A expression induces cerebral small vessel disease-related phenotypes

Project description:Cerebral small vessel disease (cSVD) is the most common cause of vascular cognitive impairment and dementia (VCID) and highly associated with Alzheimer’s disease pathogenesis. There is an urgent need to establish relevant animal models for cSVD. As aging is the strongest risk factor for these diseases, cerebrovascular senescence is implicated in cSVD pathogenesis. We investigated how AAV-based expression of senescence marker CDKN2A/p16INK4A in cerebrovascular endothelial cells influences cSVD phenotypes in adult wild-type mice. A single intraperitoneal injection of the AAV carrying CDKN2A/p16INK4A caused blood-brain barrier impairments, neurovascular uncoupling, and reduction of cerebral blood flow, accompanied with behavioral changes in mice. While single cell RNA-sequencing and immunostaining revealed the upregulation of VCAM1 in cerebrovascular endothelial cells, in vivo two-photon excitation microscopy detected aggravated leukocyte adhesions to capillaries. Our findings demonstrate the contributions of p16INK4A in cerebrovascular endothelial cells to cSVD and VCID pathogenesis through new mouse model.

2025-08-20 | GSE304696 | GEO

Entamoeba histolytica extracellular vesicles drive pro-inflammatory monocyte signaling

Project description:The parasitic protozoan Entamoeba histolytica secretes extracellular vesicles (EVs), but so far little is known about their function in the interaction with the host immune system. Infection with E. histolytica trophozoites can lead to formation of amebic liver abscesses (ALAs), in which pro-inflammatory immune responses of Ly6Chi monocytes contribute to liver damage. Men exhibit a more severe pathology as the result of higher monocyte recruitment and a stronger immune response. To investigate the role of EVs and pathogenicity in the host immune response, we studied the effect of EVs secreted by low pathogenic EhA1 and highly pathogenic EhB2 amebae on monocytes. Size and quantity of isolated EVs from both clones were similar. However, they differed in their proteome and miRNA cargo, providing insight into factors potentially involved in amebic pathogenicity. In addition, EVs were enriched in proteins with signaling peptides compared with the total protein content of trophozoites. Exposure to EVs from both clones induced monocyte activation and a pro-inflammatory immune response as evidenced by increased surface presentation of the activation marker CD38 and upregulated gene expression of key signaling pathways (including NF-B, IL-17 and TNF signaling). The release of pro-inflammatory cytokines was increased in EV-stimulated monocytes and more so in male- than in female-derived cells. While EhA1 EV stimulation caused elevated myeloperoxidase (MPO) release by both monocytes and neutrophils, EhB2 EV stimulation did not, showing the protective role of MPO during amebiasis. Collectively, our results suggest that parasite-released EVs contribute to the male-biased immunopathology mediated by pro-inflammatory monocytes during ALA formation.

2025-03-06 | PXD059636 | Pride

Increased pro-inflammatory phenotype of peripheral blood monocytes and monocyte-derived macrophages among patients with excessive ethanol intake

Project description:Increased pro-inflammatory phenotype of peripheral blood monocytes and monocyte-derived macrophages among patients with excessive ethanol intake

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Deoxyhypusine Synthase Promotes a Pro-Inflammatory Macrophage Phenotype

Project description:Deoxyhypusine Synthase Promotes a Pro-Inflammatory Macrophage Phenotype

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Dietary intake regulates the circulating pro-inflammatory monocyte pool

Project description:Dietary intake regulates the circulating pro-inflammatory monocyte pool

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Attenuated inflammatory profile following single and repeated handgrip exercise and remote ischemic preconditioning in patients with cerebral small vessel disease

Project description:Similar to remote ischemic preconditioning bouts of exercise may possess immediate protective effects against ischemia-reperfusion injury. However, underlying mechanisms are largely unknown. This study compared the impact of single and repeated handgrip exercise versus remote ischemic preconditioning on inflammatory biomarkers in patients with cerebral small vessel disease (cSVD). In this crossover study, 14 patients with cSVD were included. All participants performed 4-days of handgrip exercise (4x5-minutes at 30% of maximal handgrip strength) and remote ischemic preconditioning (rIPC; 4x5-minutes cuff occlusion around the upper arm) twice daily. Patients were randomized to start with either handgrip exercise or rIPC and the two interventions were separated by >9 days. Venous blood was drawn before and after one intervention, and after 4-days of repeated exposure. We performed a targeted proteomics on inflammation markers in all blood samples.

2023-03-11 | PXD037267 | Pride

Effect of GSK3 inhibition on the transcriptional signature of human GM-CSF-dependent monocyte-derived macrophages

Project description:The functional versatility of macrophages is intrincately tied to factors such as their ontogeny and the specific tissue and extracellular environment. Monocyte-derived macrophages are oppositely instructed by M-CSF or GM-CSF. GM-CSF drives monocyte-derived macrophages towards heightened pro-inflammatory activity and the acquisition of the lung alveolar macrophage phenotype and gene profile whereas M-CSF gives rise to anti-inflammatory, pro-resolving, and immunosuppressive monocyte-derived macrophages. We explored the molecular impact of blocking GSK3 on the gene expression profile in GM-CSF-primed human monocyte derived macrophages. GSK3 inhibition skewed the transcriptional profile of GM-MØ towards an anti-inflammatory phenotype.

2025-04-16 | GSE256208 | GEO

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