Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Inflammatory responses revealed through HIV infection of microglia-containing cerebral organoids

ABSTRACT: Inflammatory responses revealed through HIV infection of microglia-containing cerebral organoids

PROVIDER: PRJNA1189530 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR31463151_1.fastq.gz	Fastqsanger.gz
	SRR31463151_2.fastq.gz	Fastqsanger.gz
	SRR31463152_1.fastq.gz	Fastqsanger.gz
	SRR31463152_2.fastq.gz	Fastqsanger.gz
	SRR31463153_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 24

Similar Datasets

Inflammatory responses revealed through HIV infection of microglia-containing cerebral organoids

Project description:Cerebral organoids (COs) are valuable tools for studying the intricate interplay between glial cells and neurons in brain development and disease, including HIV-associated neuroinflammation. We developed a novel approach to generate microglia containing COs (CO-iMs) by coculturing hematopoietic progenitors and inducing pluripotent stem cells from the same line. This approach allowed for the differentiation of microglia within the organoids concomitantly with the neuronal progenitors. Compared with conventional COs, CO-iMs were more efficient at generating CD45+/CD11b+/Iba-1+ microglia and presented a physiologically relevant proportion of microglia (~7%). CO-iMs presented substantially increased expression of microglial homeostatic and sensome markers as well as markers for the complement cascade. CO-iMs are susceptible to HIV infection, resulting in a significant increase in several pro-inflammatory cytokines/chemokines and compromised neuronal functions, which are abrogated by the addition of antiretrovirals. Thus, CO-iM is a robust model for deciphering neuropathogenesis, neurological disorders, and viral infections of brain cells in a 3D culture system.

2025-02-19 | GSE282644 | GEO

A microglia-containing cerebral organoid model to study early life immune challenges [scRNA-seq]

Project description:Prenatal infections and activation of the maternal immune system have been proposed to contribute to causing neurodevelopmental disorders (NDDs), chronic conditions often linked to brain abnormalities. Microglia are the resident immune cells of the brain and play a key role in neurodevelopment. Disruption of microglial functions can lead to brain abnormalities and increase the risk of developing NDDs. How the maternal as well as the fetal immune system affect human neurodevelopment and contribute to NDDs remains unclear. An important reason for this knowledge gap is the fact that the impact of exposure to prenatal risk factors has been challenging to study in the human context. Here, we characterized a model of cerebral organoids (CO) with integrated microglia (COiMg). These organoids express typical microglial markers and respond to inflammatory stimuli. The presence of microglia influences cerebral organoid development, including cell density and neural differentiation, and regulates the expression of several ciliated and mesenchymal cell markers. Moreover, COiMg and organoids without microglia show similar but also distinct responses to inflammatory stimuli. Additionally, IFN-γ induced significant transcriptional and structural changes in the cerebral organoids, that appear to be regulated by the presence of microglia. Specifically, interferon-gamma (IFN-γ) was found to alter the expression of genes linked to autism. This model provides a valuable tool to study how inflammatory perturbations and microglial presence affect neurodevelopmental processes.

2025-01-29 | GSE281452 | GEO

A microglia-containing cerebral organoid model to study early life immune challenges [Bulk RNA-seq]

2025-01-29 | GSE281451 | GEO

A microglia-containing cerebral organoid model to study early life immune challenges [scRNA-seq]

Project description:A microglia-containing cerebral organoid model to study early life immune challenges [scRNA-seq]

| PRJNA1183880 | ENA

Dysregulated neuroimmune interactions and sustained type I interferon signaling after human immunodeficiency virus type 1 infection of human iPSC derived microglia and cerebral organoids

Project description:Human immunodeficiency virus type-1 (HIV-1) associated neurocognitive disorder (HAND) affects up to half of HIV-1 positive patients with long term neurological consequences, including dementia. There are no effective therapeutics for HAND because the pathophysiology of HIV-1 induced glial and neuronal functional deficits in humans remains enigmatic. To bridge this knowledge gap, we established a model simulating HIV-1 infection in the central nervous system using human induced pluripotent stem cell (iPSC) derived microglia combined with sliced neocortical organoids. Upon incubation with two replication-competent macrophage-tropic HIV-1 strains (JRFL and YU2), we observed that microglia not only became productively infected but also exhibited inflammatory activation. RNA sequencing revealed a significant and sustained activation of type I interferon signaling pathways. Incorporating microglia into sliced neocortical organoids extended the effects of aberrant type I interferon signaling in a human neural context. Collectively, our results illuminate the role of persistent type I interferon signaling in HIV-1 infected microglial in a human neural model, suggesting its potential significance in the pathogenesis of HAND.

2023-10-25 | GSE246082 | GEO

HIV-1 integration in microglia

Project description:HIV-1 integration in microglia

| PRJNA848224 | ENA

A microglia-containing cerebral organoid model to study early life immune challenges [Bulk RNA-seq]

Project description:A microglia-containing cerebral organoid model to study early life immune challenges [Bulk RNA-seq]

| PRJNA1183876 | ENA

Transcriptional changes following HIV infection of choroid plexus brain organoids

Project description:We employed iPSC-derived choroid plexus brain organoids to explore the impact of HIV infection on microglia, elucidating alterations in the host gene profile within the central nervous system. We conducted single-cell RNA sequencing to elucidate the changes in microglia upon HIV infection, leading to neural cell damage

2024-04-29 | GSE262349 | GEO

Transcriptomic profiling of microglia from a model of Experimental Cerebral Malaria Transcriptomic profiling of microglia from a model of Experimental Cerebral Malaria

Project description:Cerebral malaria is a pathology involving inflammation in the brain. There are many immune cell types activated during this process, but there is little information on the contribution of microglia, the brain resident macrophages, to this severe complication. We have examined the responses of microglia in a model of experimental cerebral malaria (ECM), in which C57BL/6 mice are infected with Plasmodium berghei ANKA. Genome wide transcriptomic analysis of these cells revealed that thousands of transcripts were differentially expressed at two different time points during the infection. The analysis indicated that proliferation of microglia was a dominant feature before the onset of ECM, and supporting this, we observed an increase in numbers of these cells in the brain. When cerebral malaria symptoms were manifest, genes involved in immune responses and chemokine production were upregulated, which were possibly driven by Type I Interferon. Together, our data offer a unique insight into the responses of microglia in the brain during ECM.

2016-12-19 | GSE86082 | GEO

HIV-1 integration in microglia (ATAC-seq)

Project description:We performed ATAC-seq in a microglia cell line (C20) to assess chromatin accessibility alterations upon HIV-1 infection in latent and active status in comparison with the uninfected status.

2023-02-20 | GSE205807 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data