Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

ABSTRACT: Trancriptional signatures of dexamethasone-treated sarcoidosis alveolar macrophages (AMs)

PROVIDER: PRJNA630000 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR11670479_1.fastq.gz	Fastqsanger.gz
	SRR11670479_2.fastq.gz	Fastqsanger.gz
	SRR11670480_1.fastq.gz	Fastqsanger.gz
	SRR11670480_2.fastq.gz	Fastqsanger.gz
	SRR11670481_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 39

Similar Datasets

Trancriptional signatures of dexamethasone-treated sarcoidosis alveolar macrophages (AMs)

Project description:The goal of this study was to determine the effect of dexamethasone treatment on trancriptional signatures and pathways of sarcoidosis AMs.

2020-05-20 | GSE150842 | GEO

Trancriptional signatures of dexamethasone-treated sarcoidosis monocytes.

Project description:Trancriptional signatures of dexamethasone-treated sarcoidosis monocytes.

| PRJNA630995 | ENA

Trancriptional signatures of dexamethasone-treated sarcoidosis monocytes.

Project description:The goal of this study was to determine the effect of dexamethasone treatment on trancriptional sigantures and pathways of sarcoidosis monocytes.

2020-05-20 | GSE150049 | GEO

Transcriptional characterization of mononuclear phagocytes (MNP) in blood and BAL of healthy and sarcoidosis patients

Project description:Pulmonary sarcoidosis is an inflammatory disease characterized by granuloma formation and heterogeneous clinical outcome. TNF is a proinflammatory cytokine contributing to granuloma formation and high levels of TNF have been shown to associate with progressive disease. Mononuclear phagocytes (MNPs) are potent producers of TNF and highly responsive to inflammation. In sarcoidosis, alveolar macrophages (AMs) have been well studied. However, MNPs also include monocytes/monocyte-derived cells and dendritic cells (DCs) that despite their central role in inflammation are poorly studied in sarcoidosis. We performed in-depth phenotypic, functional and transcriptomic analysis of MNPs subsets from blood and bronchoalveolar lavage (BAL) fluid from 108 sarcoidosis patients and 30 healthy controls.

2021-05-19 | GSE174659 | GEO

Alterations in the membrane-associated proteome of alveolar macrophages in sarcoidosis

Project description:Here we have performed qualitative profiling of the membrane-associated proteome of alveolar macrophages in sarcoidosis patients and healthy individuals with the aim to identify specific proteins and pathways involved in sarcoidosis pathology.

2016-12-23 | PXD000752 | Pride

Transcriptional profiling of primary human alveolar macrophages challenged with Streptococcus pneumoniae from patients with chronic obstructive pulmonary disease compared to healthy donors

Project description:Transcriptional profiling of primary human alveolar macrophages (AMs) comparing control untreated AMs with AMs exposed with Serotype 14 Streptococcus pneumoniae (NCTC11902) strain (MOI 10) for 4 hours) Two-condition experiment, control AMs vs. infected AMs. Biological replicates: 3 control replicates, 3 infected replicates MOI 10.

2018-02-26 | E-MTAB-6491 | biostudies-arrayexpress

RNA-seq of mouse alveolar macrophages sorted from CD11cCre/+ Tgfbr2fl/fl and control Tgfbr2fl/fl neonatal mice

Project description:Alveolar macrophages (AMs) are lung resident phagocytes. They derive from fetal liver monocytes, which colonize the lung during embryonic development and give rise to fully mature AMs perinatally. We have identified TGF- signaling as an indispensible regulator during this process. To analyze the impact of TGF- on the entire transcriptome of AMs, we performed RNA-seq on AMs deficient of Tgfbr2 in CD11cCre/+ Tgfbr2fl/fl mice at P3 with Tgfbr2fl/fl littermates as a control.

2017-11-08 | E-MTAB-6028 | biostudies-arrayexpress

Control of alveolar macrophage differentiation by Siah1a/2 ubiquitin ligases limits carcinogen-induced lung adenocarcinoma [Bulk RNA-seq]

Project description:Tumor microenvironment components, including T and myeloid cells, play important roles in lung adenocarcinoma (LADC) progression and response to therapy. Here, we identify a role for Siah1a/2 ubiquitin ligases in controlling alveolar macrophage (AM) differentiation and urethane-induced LADC. Genetic ablation of Siah1a/2 in AMs enriched their immature state, coinciding with increased pro-tumorigenic and inflammatory gene signatures and abundance of Siah1a/2 substrates NRF2 and B-catenin. Urethane administration to mice enriched the population of monocytic and immature-like AMs, which were more prevalent in the lungs of mice carrying Siah1a/2-ablated macrophages. While resembling transitional profibrotic macrophages often seen in lung fibrosis, enrichment of immature AMs coincided with the development of more frequent and larger lung tumors in urethane-treated mice harboring Siah1a/2 ablated macrophages compared with controls. Gene expression signature of Siah1a/2 ablated immature-like AMs is associated with increased infiltration of CD14+ immune cells and worse survival of LADC patients. Our findings identify Siah1a/2 as gatekeepers of cancer development by controlling AM differentiation and profibrotic phenotypes contributing to carcinogen-induced lung cancer.

2023-05-15 | GSE215920 | GEO

Control of alveolar macrophage differentiation by Siah1a/2 ubiquitin ligases limits carcinogen-induced lung adenocarcinoma [scRNA-seq]

2023-05-15 | GSE215992 | GEO

SARS-CoV-2 Evades immune detection in Alveolar Macrophages

Project description:Respiratory infections, like the current pandemic SARS-CoV-2 virus, target the epithelial cells in the respiratory tract. However, alveolar macrophages (AMs) are tissue-resident macrophages located within the alveoli of the lung and they play a key role in the early phases of an immune response to respiratory infections. We expect that AMs are the first immune cells to encounter the SARS-CoV-2 and therefore their reaction to SARS-CoV-2 infection will have a profound impact upon the outcome of the infection. Interferons (IFNs) are antiviral cytokines and the first cytokine produced upon viral infection. Here, we challenge AMs with SARS-CoV-2 and to our surprise find that the AMs are incapable of recognising SARS-CoV-2 and produce IFN. This is in contrast to respiratory pathogens, such as influenza A virus and Sendai virus. Callenge of AMs with those viruses resulted in a robust IFN response. The absence of IFN production by AMs upon challenge could explain the initial asymptotic phase of SARS-CoV-2 infections and argues against the AMs as the source of proinflamatory cytokines later in infection.

2020-10-20 | PXD021685 | Pride

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