Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Gene expression profile at single cell level of murine macrophages infected with Mtb (-/+ TLR2)

ABSTRACT: Gene expression profile at single cell level of murine macrophages infected with Mtb (-/+ TLR2)

PROVIDER: PRJNA971605 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR24512177.fastq.gz	Fastqsanger.gz
	SRR24512178.fastq.gz	Fastqsanger.gz
	SRR24512179_1.fastq.gz	Fastqsanger.gz
	SRR24512179_2.fastq.gz	Fastqsanger.gz
	SRR24512180_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 6

Similar Datasets

Gene expression profile at single cell level of murine macrophages infected with Mtb (-/+ TLR2)

Project description:The macrophage is a cellular reservoir for Mtb infection. We profiled BMDM following Mtb infection.

2023-06-01 | GSE232320 | GEO

Gene expression profile at single cell level of mice infected with Mtb (-/+ TLR2)

Project description:Gene expression profile at single cell level of mice infected with Mtb (-/+ TLR2)

| PRJNA953385 | ENA

Gene expression profile at single cell level of mice infected with Mtb (-/+ TLR2)

Project description:The lung is a key site of Mtb infection. We profiled the lung ecosystem of mice following Mtb infection.

2023-06-03 | GSE229190 | GEO

miRNA profiles of Mtb H37Rv infected peritoneal macrophages and uninfected controls

Project description:The peritoneal macrophages were infected with Mtb H37Rv for 4 hours, and the miRNA expression profile were analyzed with deep sequencing.

2018-09-06 | GSE119495 | GEO

Impact of Wnt6 knockout in Mtb infected murine BMDM

Project description:In view of emerging drug-resistant tuberculosis, host directed therapies are urgently needed to improve treatment outcomes with currently available anti-tuberculosis therapies. One option is to interfere with the formation of lipid-laden “foamy” macrophages in the infected host. Here, we provide evidence that WNT6, a member of the evolutionary conserved WNT signaling pathway, promotes foam cell formation by regulating key lipid metabolic genes including acetyl-CoA carboxylase-2 (ACC2) during pulmonary TB. In addition, we demonstrate that Mycobacterium tuberculosis (Mtb) facilitates its intracellular growth and dissemination in the host by exploiting the WNT6-ACC2 pathway. Using genetic and pharmacological approaches, we show that lack of functional WNT6 or ACC2 significantly reduces intracellular TAG levels, Mtb growth and necrotic cell death of macrophages. In combination with the anti-TB drug isoniazid, pharmacological inhibition of ACC2 improved anti-mycobacterial treatment in vitro and in vivo. Therefore, we propose the WNT6-ACC2 signaling pathway as a promising target for a host-directed therapy to reduce intracellular replication of Mtb by modulating neutral lipid metabolism.

2021-06-01 | GSE160039 | GEO

Metabolic transcriptional profile of virulent Mtb-infected human AM

Project description:Mycobacterium tuberculosis (Mtb)-induced shifts in macrophage metabolism are an accepted central infection paradigm. Mtb-infected murine lung tissue exhibits gene expression changes consistent with classic Warburg metabolism and Mtb-infected murine macrophages undergo TCA cycle remodeling. Human macrophages also respond energetically to Mtb infection, however, interestingly the phenotypic nature of this response appears to vary depending on the viability of infection. Despite the overwhelming consensus that metabolic changes are critical to the host response to infection, we have little understanding of the metabolic transcriptional landscape of virulent Mtb-infected human alveolar macrophages (AM), the sentinel pulmonary immune cell during Mtb infection. Further still, whether the human AM undergoes glycolytic reprogramming and TCA cycle remodeling during virulent Mtb infection remains undefined; as is suggested to occur in circulating Mtb-infected human macrophages. Here, we aimed to characterise the metabolic transcriptional profile of virulent Mtb-infected human AM. We hypothesised that infection would induce the transcriptome of Warburg metabolism (characterised by aerobic glycolysis), TCA cycle remodeling, and reduce expression of genes involved in mitochondrial oxidative phosphorylation (OXPHOS).

2025-05-15 | GSE266414 | GEO

Profiling of gene expression in TLR2 and TLR3 activated macrophages

Project description:We have identified more than 50 genes that have upregulated expression in TLR3 activated (PMI-1,2), but have downregulated expression in TLR2 activated (PMP-1,2) macrophages, as compared to control cells (PMC-1,2) identify genes that have upregulated expression in TLR3 activated (PMI-1,2), but have downregulated expression in TLR2 activated (PMP-1,2) macrophages, as compared to control cells (PMC-1,2)

2012-03-27 | E-GEOD-36891 | biostudies-arrayexpress

TLR2 dimerization blockade allows generation of homeostatic intestinal macrophages under acute colitis challenge

Project description:Recruited blood monocytes contribute to the establishment, perpetuation and resolution of tissue inflammation. Specifically, in the inflamed intestine, monocyte ablation was shown to ameliorate colitis scores in preclinical animal models. However, the majority of intestinal macrophages that seed the healthy gut are also monocyte-derived. Monocyte ablation aimed to curb inflammation would therefore likely interfere with intestinal homeostasis. Here, we used a TLR2 trans-membrane peptide which blocks TLR2 dimerization that is critical for TLR2 /1 and TLR2 / 6 heterodimer signaling to blunt inflammation in a murine colitis model. We show that while the TLR2 peptide treatment ameliorated colitis, it allowed recruited monocytes to give rise to macrophages that lack the detrimental pro-inflammatory gene signature and reduced potentially damaging neutrophils infiltrates. Finally, we demonstrate TLR blocking activity of the peptide on in vitro cultured human monocyte-derived macrophages. Collectively, we provide a significantly improved anti-inflammatory TLR2 peptide and critical insights in its mechanism of action towards future potential use in the clinic.

2019-11-24 | GSE140788 | GEO

Ubiquitination Proteome of heat-killed MTB stimulated Thp-1-derived macrophages

Project description:This project analyzed the ubiquitination proteome of heat-killed MTB stimulated and unstimulated macrophages.

2023-02-07 | PXD039906 |

miRNA profile of THP-1 macrophage infected with different MTB strains

Project description:We examined the microRNA profiles of THP-1 macrophages upon the MTB infection of (1) Beijing/W and non-Beijing/W clinical strains, and (2) susceptible and multidrug-resistant (MDR-) MTB strains.

2015-07-01 | GSE65811 | 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