Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

A virus-specific monocyte inflammatory phenotype is induced by SARS-CoV2 at the immune-epithelial interface

ABSTRACT: A virus-specific monocyte inflammatory phenotype is induced by SARS-CoV2 at the immune-epithelial interface

PROVIDER: PRJNA774966 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR16596100_1.fastq.gz	Fastqsanger.gz
	SRR16596100_2.fastq.gz	Fastqsanger.gz
	SRR16596200_1.fastq.gz	Fastqsanger.gz
	SRR16596200_2.fastq.gz	Fastqsanger.gz
	SRR16596300_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 568

Similar Datasets

A virus-specific monocyte inflammatory phenotype is induced by SARS-CoV2 at the immune-epithelial interface

Project description:RNAseq analysis of human immune cells (monocytes CD14+ and B cells CD19+) cocultured with SARS-CoV2, influenza A or Ebola viruses-infected epithelial cells as well as directly infected or SARS-CoV2 single protein transfected epithelial cells

2021-10-29 | GSE186650 | GEO

Bulk RNA-seq of an ALI (Air-lung interface) model of SARS-CoV2

Project description:This dataset looks at the transcriptome of in vitro-differentiated primary lung cells infected with SARS-CoV2. Some cells have been treated with the drug Enzalutamide.

2022-05-04 | E-MTAB-10687 | biostudies-arrayexpress

Single-cell RNA-seq of an ALI (Air-lung interface) model of SARS-CoV2

Project description:This dataset looks at the transcriptome of in vitro-differentiated primary lung cells during an infection time course of SARS-CoV2. Some cells have been treated with the drug Enzalutamide. Cells from one man and one female were mixed to minimize the technical variability, and can be separated by SNPs (SNPs not included, but the calculated cell-donor associations are provided).

2023-04-01 | E-MTAB-10697 | biostudies-arrayexpress

SARS-CoV2 infection triggers reactive astrocyte states and inflammatory conditions in Human Cortical Organoids

Project description:SARS-CoV2, severe acute respiratory syndrome coronavirus 2, is frequently associated with neurological manifestations. Despite the presence of mild to severe CNS-related symptoms in a cohort of patients, there is no consensus whether the virus can infect directly brain tissue or if the symptoms in patients are a consequence of peripheral infectivity of the virus. Here, we use a human stem cell-derived cortical organoid model to assess SARS-CoV2 infectivity of brain cells and unravel the cell-type tropism and its downstream pathological effects. Our results show consistent and reproducible low levels of SARS-CoV2 infection in human cortical organoids at different maturation stages in vitro. We found that astrocytes, deep projection neurons, upper callosal neurons and inhibitory neurons were infected by SARS-CoV2. Interestingly, astrocytes showed the highest infection rate among all infected cell populations that led to increased presence of reactive states. Further, transcriptomic analysis revealed overall changes in expression of genes related to oxidative phosphorylation, TNFA signaling, astrocyte activation and metabolic changes. Thus, local and minor infectivity of SARS-CoV2 in the brain may induce widespread adverse effects in brain cell populations.

2025-02-28 | GSE250289 | GEO

SARS-COV2 study

Project description:SARS-COV2 Sequencing Study

| PRJEB58341 | ENA

Bulk RNA-seq of an ALI (Air-lung interface) model of SARS-CoV2

Project description:Bulk RNA-seq of an ALI (Air-lung interface) model of SARS-CoV2

| PRJEB52612 | ENA

Transcriptomics analysis of SARS-CoV2-induced changes in human lung epithelial Calu-3 cells

Project description:RNA-Seq was carried out in order to obtain the time dependent expression dynamics of SARS-CoV2 (Trondheim strain)-induced transcriptome changes in human lung epithelial Calu-3 cells.

2022-10-25 | E-MTAB-12134 | biostudies-arrayexpress

IL-9 exacerbates SARS-CoV2 infection and associated airway inflammation

Project description:Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) causes coronavirus diseases 2019 (COVID-19) and broncho-alveolar inflammation (Merad and Martin, 2020). IL-9 induces airway inflammation and bronchial hyper responsiveness in respiratory viral illnesses and allergic inflammation (Temann et al., 1998). However, the role of IL-9 is not yet identified in SARS-CoV2 infection. Here we show that IL-9 promotes SARS-CoV2 infection and airway inflammation in K18-hACE2 transgenic (ACE2.Tg) mice, as IL-9 blockade reduces SARS-CoV2 infection and suppressed airway inflammation. Foxo1 is essential for the induction of IL-9 in helper T (Th) cells (Malik et al., 2017). While ACE2.Tg mice with Foxo1-deficiency in CD4+ T cells were performed to be resistant to SARS-CoV2 infection associated with reduced IL-9 production, exogenous IL-9 made Foxo1-deficient mice susceptible to SARS-CoV2 infection with increased airway inflammation. Collectively, we identify a mechanistic insight of IL-9-mediated regulation of antiviral and inflammatory pathways in SARS-CoV2 infection, and unravel a principle for the development of host-directed therapeutics to mitigate disease severity.

2022-07-22 | GSE209550 | GEO

Single-cell RNA-seq of an ALI (Air-lung interface) model of SARS-CoV2

Project description:Single-cell RNA-seq of an ALI (Air-lung interface) model of SARS-CoV2

| PRJEB52725 | ENA

Single-cell RNA-seq of an ALI (Air-lung interface) model of SARS-CoV2

Project description:Single-cell RNA-seq of an ALI (Air-lung interface) model of SARS-CoV2

| PRJEB53344 | ENA