Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Timecourse of C56BL6 BMDM stimulated with different TLRs (part-I)

ABSTRACT: C57BL6 bone marrow derived macrophages were stimulated with TLR2, TLR3, TLR4, TLR7, and TLR9 ligands for 24 or 48 h.

ORGANISM(S): Mouse Mus Musculus

TISSUE(S): Macrophages

SUBMITTER: Steven Bensinger

PROVIDER: ST001342 | MetabolomicsWorkbench | Fri Mar 27 00:00:00 GMT 2020

REPOSITORIES: MetabolomicsWorkbench

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	mwtab	Other

Items per page:

1 - 1 of 1

Similar Datasets

C56BL6 BMDM stimulated with different TLRs W/O acetylated LDL (part-II)

Project description:C57BL6 bone marrow derived macrophages were preloaded with 50 ug/mL of acetylated LDL and stimulated with TLR2, TLR3, TLR4, TLR7, and TLR9 ligands for 48 h.

2020-04-01 | ST001341 | MetabolomicsWorkbench

C56BL6 WT or IFNARKO BMDM stimulated with different TLRs (part-V)

Project description:WT control or IFNAR deficient bone marrow derived macrophages were stimulated with IFNb, TLR3, IFNg, TLR4, and TLR4+IFNg ligands for 48 h.

2020-04-01 | ST001345 | MetabolomicsWorkbench

C56BL6 WT or TRIFKO BMDM stimulated with different TLRs (part-III)

Project description:WT control or TRIF deficient bone marrow derived macrophages were stimulated with TLR2, TLR3, and TLR4 ligands for 48 h.

2020-04-01 | ST001343 | MetabolomicsWorkbench

C56BL6 WT or MyD88KO BMDM stimulated with different TLRs (part-IV)

Project description:WT control or MyD88 deficient bone marrow derived macrophages were stimulated with TLR2, TLR3, TLR4, TLR7, and TLR9 ligands for 48 h.

2020-04-01 | ST001344 | MetabolomicsWorkbench

Comparison of gene expression in macrophages tolerised by different toll-like receptor ligands

Project description:To investigate the similarity of toll-like receptor tolerance in macrophages stimulated with different toll-like receptor ligands we stimulated naïve or tolerant macrophages with ligands for TLR4, TLR2, TLR3 and TLR9. The data identifies a core set of genes that are tolerised by all ligands and genes that show TLR specific patterns.

2018-05-30 | GSE81291 | GEO

miRNA profiles in unstimulated and TLR stimulated MDMs

Project description:Macrophages play a crucial role in HIV-1 pathogenesis. Toll-like receptors (TLRs) are fundamental for innate and adaptive immune responses, but their role in HIV-1 infection is still incompletely understood. The TLR3 and TLR4 ligands poly(I:C) and LPS are known to modulate HIV-1 infection of and replication in monocyte-derived macrophages (MDMs), but the mechanism is incompletely understood. We found that MDMs stimulation with poly(I:C) or LPS abrogated infection by CCR5-using, macrophage-tropic HIV-1, or by VSV-G-pseudotyped HIV-1 virions, while TLR7 and TLR9 agonists Imiquimod and CpG only reduced infection to varying extent. Suppression of infection, or lack thereof, did not correlate with differential effects on CD4 or CCR5 expression, type I interferon induction, or production of pro-inflammatory cytokines. Furthermore, integrated pro-viruses were readily detected in unstimulated, TLR7- and TLR9-stimulated cells, but not in TLR3- or TLR4-stimulated MDMs, suggesting the alteration of post-entry, pre-integration event(s). MicroRNA (miRNA) microarray and real time PCR demonstrated increased miR-155 levels in MDMs upon TLR3/4, but not TLR7, stimulation, and a miR-155 inhibitor partially restored infectivity in poly(I:C)-stimulated MDMs. Finally, miR-155 over-expression in MDMs and cell lines remarkably diminished HIV-1 infection, inducing an accumulation of late reverse transcription products, concurrently with a decrease in mRNA levels of several HIV-1 dependency factors involved in nuclear import of pre-integration complexes. Our results suggest that miR-155 may target mRNA(s) for host cell protein(s) that either participate in or facilitate post-entry, pre-integration events, resulting in severely diminished HIV-1 infection. miRNA profiles were investigated in total RNA isolated from unstimulated and TLR3-, TLR4- and TLR7-stimulated human MDMs from a single normal donor

2011-12-14 | E-GEOD-34428 | biostudies-arrayexpress

Gene expression analysis of bronchial epithelial cells stimulated by different airway pathogens.

Project description:Bronchial epithelial cells represent the first line of defense against invading airborne pathogens. They are important contributors to innate mucosal immunity and provide a variety of anti-microbial effectors. To investigate the role of epithelial cells upon infection of airway pathogens, we stimulated BEAS-2B cells for 4 h with UV-inactivated bronchial pathogens including Staphylococcus aureus, Pseudomonas aeruginosa and Respiratory Syncitial Virus (RSV) that among other receptors can strongly activate TLR2, TLR4 and TLR3, respectively. Keywords: expression profiling, response to pathogens

2007-02-27 | GSE6802 | GEO

miRNA profiles in unstimulated and TLR stimulated MDMs

2011-12-14 | GSE34428 | GEO

RNA-seq of plasmacytoid dendritic cells stimulated by TLR3, TLR4, TLR7 and TLR8

Project description:RNA-seq of plasmacytoid dendritic cells stimulated by TLR3, TLR4, TLR7 and TLR8

| PRJNA993124 | ENA

IRF1 governs the differential Interferon-Stimulated Gene responses in human monocytes and macrophages by regulating chromatin accessibility (ATAC - Differentiation)

Project description:Myeloid lineage cells use TLRs to recognize and respond to diverse microbial ligands. Although unique transcription factors dictate the outcome of specific TLR signaling, whether lineage-specific differences exist to further modulate the quality of TLR-induced inflammation remains unclear. Comprehensive analysis of global gene transcription in human monocytes, monocyte-derived macrophages and monocyte-derived dendritic cells stimulated with various TLR ligands identifies multiple lineage-specific, TLR-responsive gene programs. Monocytes are hyperresponsive to TLR7/8 stimulation that correlates with higher expression of the receptors. While macrophages and monocytes express similar levels of TLR4, macrophages, but not monocytes, upregulate Interferon-Stimulated Genes (ISGs) in response to TLR4 stimulation. We find that TLR4 signaling in macrophages uniquely engages transcription factor IRF1, which facilitates opening of ISG loci for transcription. This study provides a critical mechanistic basis for lineage-specific TLR responses and uncovers IRF1 as a master epigenetic regulator for the ISG transcriptional program in human macrophages.

2021-03-16 | GSE147306 | 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