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Vitamin D treatment of M.tb. infected macrophages

ABSTRACT: As macrophages are the primary site of Mtb infection and are sites of vitamin D signaling, we have used these cells to understand the molecular mechanisms underlying modulation of the immune response by the hormonal form of vitamin D, 1,25-dihydroxyvitamin D (1,25D). Microarrays were used to measure the changes in gene expression induced by 1,25D treatment of H37Rv-infected THP-1 cells

ORGANISM(S): Homo sapiens

PROVIDER: GSE52819 | GEO | 2013/11/28

SECONDARY ACCESSION(S): PRJNA230131

REPOSITORIES: GEO

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Vitamin D treatment of M.tb. infected macrophages

Project description:As macrophages are the primary site of Mtb infection and are sites of vitamin D signaling, we have used these cells to understand the molecular mechanisms underlying modulation of the immune response by the hormonal form of vitamin D, 1,25-dihydroxyvitamin D (1,25D). Microarrays were used to measure the changes in gene expression induced by 1,25D treatment of H37Rv-infected THP-1 cells Cells were infected at an MOI of 5 or left uninfected, and treated with 10^-7 M 1,25D for 24 hours

2013-11-28 | E-GEOD-52819 | biostudies-arrayexpress

Vitamin D receptor (VDR) target genes in THP-1 monocytic leucemia cells

Project description:The biologically active form of vitamin D, 1,25-dihydroxyvitamin D3 (1,25(OH)2D3), is a direct regulator of gene transcription, since it is the only high affinity natural ligand of the transcription factor vitamin D receptor (VDR). Transcriptome-wide analysis of THP-1 human monocyte-like cells had indicated more than 600 genes to be significantly (p < 0.05) regulated after a 4 h stimulation with 1,25(OH)2D3. In this study, we screened of the list of primary vitamin D targets for genes encoding for transcriptional regulators and selected those of the activating transcription factor NFE2 and the transcriptional repressor BCL6. Both genes are under the control of two VDR loci and are the only 1,25(OH)2D3 targets within their respective chromosomal domain. However, NFE2 mRNA was rapidly up-regulated, while the increase of BCL6 expression showed a slower rise. After 24 h incubation of THP-1 cells with 1,25(OH)2D3 more than 1,500 genes responded significantly (p < 0.001), of which 132 where more than 2-fold induced. Public chromatin immunoprecipitation-sequencing datasets suggested that the majority of these genes could be targets of NFE2 or BCL6. In time course experiments we displayed for representative gene examples the specific delayed response of secondary 1,25(OH)2D3 targets and confirmed for the respective chromosomal domains the genomic binding of NFE2, BCL6 and VDR. In conclusion, our study indicated that the physiological response of monocytes to 1,25(OH)2D3 involves the action of NFE2 and BCL6. THP-1 cells were treated 24 h either with 0.1% ethanol (vehicle, control) or 1?,25(OH)2D3 (1,25D)

2015-04-26 | E-GEOD-60102 | biostudies-arrayexpress

Mapping Variation in Cellular and Transcriptional Response to 1,25-dihydroxyvitamin D3 in Peripheral Blood Mononuclear Cells

2016-07-01 | GSE82023 | GEO

Temporal response of Mycobacterium tuberculosis H37Rv to vitamin C exposure in THP-1 macrophages.

Project description:Transcriptional profiling of Mtb H37Rv infected into THP-1 macrophage cell line and treated with 100 µM vitamin C (vit C) for 96 hours and 144 hours, compared to gene expression profile of untreated bacteria post-infection.

2021-10-01 | GSE179376 | GEO

Transcriptomics of vitamin D treatment effects in Mycobacterium tuberculosis-infected THP-1 cells

Project description:Previous reports have shown low vitamin D serum levels and polymorphisms in the vitamin D receptor (VDR) to be associated with increased risk for TB. Given that 1?,25-dihydroxyvitamin D3 has a role in lipid metabolism control, we tested whether the link between 1?,25-dihydroxyvitamin D3 and tuberculosis involves macrophage lipid metabolism. Since formation of lipid droplets (LD) is a hallmark of lipid dysregulation in M. tuberculosis-infected macrophages, we measured LD content as a readout of altered lipid metabolism in infected THP-1 cells. Induction of LD, which peaked by 24 hours post-infection was prevented by addition of 1?,25-dihydroxyvitamin D3 at the time of infection. To investigate the mechanism of 1?,25-dihydroxyvitamin D3 modulation of LD formation, we analyzed the transcriptome of M. tuberculosis-infected THP-1 cells with and without 1?,25-dihydroxyvitamin D3 treatment. THP-1 cells were cultured in 24-well flat bottom plates, pre-treated with 20ng/ml PMA for 24 h, and incubated with M. tuberculosis H37Rv. After 4 hours of infection, cells were washed to remove extracellular bacteria and treated with 100 nM of 1?,25-dihydroxyvitamin D3. THP-1 cells were collected and analyzed at 24h. 3 biological replicates in each of the 4 groups were prepared: Infected, Infected plus 1?,25-dihydroxyvitamin D3, Non-infected, Non-infected plus 1?,25-dihydroxyvitamin D3.

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Mapping Variation in Cellular and Transcriptional Response to 1,25-dihydroxyvitamin D3 in Peripheral Blood Mononuclear Cells

Project description:This study characterizes the genetic basis of variation in the immunomodulatory effects of the active form of vitamin D, 1,25-dihydroxyvitamin D3 (1,25D). This was done by mapping quantitative traits of 1,25D response both at the cellular and transcriptional level in peripheral blood mononuclear cells (PBMCs). Total RNA extraced from peripheral blood mononuclear cells from 85 healthy individuals of African-African ancestry treated with 1,25D or the vehicle control, ethanol, for 6 hours.

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Multiple sclerosis cuprizone mouse model and vitamin D supplementation

Project description:Dietary supplementation of vitamin D is commonly recommended to patients with multiple sclerosis (MS). We investigated the effect of 1,25-dihydroxyvitamin-D3 (1,25-(OH)2D3) on the brain proteome in the cuprizone model during remyelination. Mice were demyelinated with dietary cuprizone for 7 weeks. The mice received intra-peritoneal injections of 1,25-(OH)2D3 or placebo twice a week, from week 6 and throughout week 10. Brain samples were taken after 7 weeks (demyelinated), after 8 weeks (1 week remyelination) and after 10 weeks (3 weeks of remyelination). The six experimental groups were labeled with TMT, mixed mode HPLC fractionation, and applied to LC-MS which enabled quantification of 5062 proteins with high confidence.

2017-08-16 | PXD002347 | Pride

mRNA-seq in VDR knockout and control THP-1 cells

Project description:The vitamin D receptor (VDR) has been knocked out in monocytic THP-1 cells after stimulation of ko and control cells with the the natural VDR ligand 1,25-dihydroxyvitamin D3 (1,25(OH)2D3), quadruplicate mRNA-seq has been performed

2021-09-06 | GSE157514 | GEO

Vitamin D receptor (VDR) target genes in THP-1 monocytic leucemia cells

2015-04-26 | GSE60102 | GEO

Vitamin D Receptor (VDR) ChIP-seq reported in "Vitamin D receptor and STAT3 cooperate to TET2-mediated acquisition of tolerogenesis"

Project description:The active form of vitamin D, 1,25-dihydroxyvitamin D3 (1,25(OH)2D3), induces stable tolerogenesis in dendritic cells (DC). This process involves the Vitamin D receptor (VDR) which translocates to the nucleus, binds its cognate genomic sites and promotes epigenetic and transcriptional remodeling. In this study, we investigated the interplay between the vitamin D receptor (VDR) and transcription factors to induce DNA methylation changes, which might provide phenotypic stability to the tolerogenic phenotype of DCs.

2022-02-23 | GSE145584 | GEO

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