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Oxygen-dependent changes of gene expression in BMDM after LPS treatment

ABSTRACT: We report oxygen-dependent changes of gene expression in BMDM after LPS treatment.

ORGANISM(S): Mus musculus

PROVIDER: GSE181641 | GEO | 2024/04/06

REPOSITORIES: GEO

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Oxygen-dependent changes of gene expression in BMDM after LPS treatment

Project description:Oxygen-dependent changes of gene expression in BMDM after LPS treatment

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Lysosome activity-dependent changes of gene expression in BMDM after LPS treatment

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Oxygen-dependent changes and lysosome activity-dependent changes of gene expression in BMDM after LPS treatment

Project description:Oxygen-dependent changes and lysosome activity-dependent changes of gene expression in BMDM after LPS treatment

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Lysosome activity-dependent changes of gene expression in BMDM after LPS treatment

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Expression data from pig BMDM treated with salmonella LPS

Project description:Mouse bone marrow-derived macrophages (BMDM) grown in macrophage colony-stimulating factor (CSF-1) have been used widely in studies of macrophage biology and the response to toll-like receptor agonists. We investigated whether similar cells could be derived from the domestic pig. Cultivation of pig bone marrow cells for 5-7 days in presence of rhCSF-1 generated a pure population of BMDM that expressed the usual macrophage markers (CD14, CD16, CD163, CD172a), are potent phagocytic cells and produced tumor necrosis factor (TNF) in response to lipopolysaccharide (LPS). Bone marrow cells could be stored frozen and thawed, providing a renewable resource. We profiled gene expression in pig BMDM from outbred animals (Large-White Landrace F1cross) responding to LPS using Affymetrix microarrays. The temporal cascade of inducible and repressible genes more closely-resembled human than mouse macrophages, and included genes involved in tryptophan metabolism (IDO, KYN), lymphoattractant chemokines (CCL20) and the vitamin D3-converting enzyme Cyp27B1. Conversely, pig BMDM, like human macrophages, did not induce genes involved in arginine metabolism, nor did they produce nitric oxide. The data establish pig BMDM as an alternative tractable model for the study of macrophage transcriptional control. RNA for gene expression analysis was collected at time points 0, 2, 7 and 24 hours post LPS stimulation (100ng/ml). Each time point included BMDM from the same three pigs and each cell culture was replicated. The replicate of the pig3_24h was not suitable for RNA analysis. Therefore, a total of 23 microarrays were hybridized.

2011-08-31 | E-GEOD-30956 | biostudies-arrayexpress

ATAC-sequencing of BTBR and C57BL6/J BMDM with Repeated LPS Treatment

Project description:The ability of peripheral innate immune cells to control pro-inflammatory cytokines during periods of repeated or prolonged exposure to immune activating stimuli is critical for preventing tissue damage. In macrophages, repeated exposure to lipopolysaccharide (LPS) induces a refractory period of immune activation termed endotoxin tolerance. Macrophages from the BTBR mouse strain have a skewed pro-inflammatory phenotype and show a hyper-response to LPS challenge. To identify disrupted regulatory mechanisms governing control of cytokine expression in BTBR compared to C57BL/6J mice (C57), we assessed bone marrow derived macrophages (BMDM) treated with either media, one dose or two doses of LPS. Differences in chromatin accessibility using ATAC-sequencing were used to identify regions of differential chromatin accessibility both under baseline media conditions and in response to LPS.

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Expression data from pig BMDM treated with salmonella LPS

2011-09-01 | GSE30956 | GEO

Oxygen-dependent changes and lysosome activity-dependent changes of gene expression in BMDM after LPS treatment

Project description:This SuperSeries is composed of the SubSeries listed below.

2024-04-06 | GSE181643 | GEO

High-throughput sequencing Analysis of mouse BMDM cell Transcriptomes after LPS Challenge

Project description:Purpose: Mouse BMDM is the universal cell type of studying innate immunity.This study was designed to analyze LPS induced innate immune respone and the gene expression in WT and HDAC3 KO BMDMs. Methods: BMDM cells from Hdac3f/f and Lyz2-Cre-Hdac3f/f were treated with or without LPS for 4 hours. Then mRNA profiles of these samles were generated by High-throughput sequencing analysis, in triplicate, using illumina HiSeqTM2000/MiSeq. And the differencial mRNA profiles were analyzed. Results: mRNA profiles were analyzed, and differencial expression profiles were compared . Conclusions: Our study demostrated the transcriptional profiles of BMDMs from Hdac3f/f and Lyz2-Cre-Hdac3f/f mice upon LPS challenge, with biologic replicates, generated by RNA-seq technology.

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Gene expression in LPS stimulated IkappaB-beta knockout bone marrow derived macrophage (BMDM)

Project description:Inflammation is beneficial when it is part of the innate immune response, but harmful when it occurs in an unregulated, chronic manner. We now report that IkappaB-beta, a member of the classical IkappaB family, serves a dual role of both inhibiting and facilitating the inflammatory response. IkappaB-beta degradation releases NF-kappaB dimers which upregulate proinflammatory target genes such as TNF-alpha. Suprisingly absence of IkappaB-beta results in a dramatic reduction of TNF-alpha in response to LPS even though the activation of NF-kappaB is normal. The inhibition of TNF-alpha mRNA expression can be correlated to the absence of nuclear, hypophosphorylated-IkappaB-beta bound to p65:cRel heterodimers at a specific kappaB site on the TNF-alpha promoter. Therefore IkappaB-beta acts through p65:cRel dimers to maintain prolonged expression of TNF-alpha. As a result, IkappaB-beta knockout mice are resistant to LPS induced septic shock and collagen-induced arthritis, and therefore blocking IkappaB-beta might be a promising new strategy for selectively inhibiting the chronic phase of TNF-alpha producting during the inflammatory response. Wild type and IkappaB-beta knockout BMDM cells were stimulated with LPS(1ug/ml) for 0, 1, and 5 hours. RNA isolated from the cells was analyzed on Affymetrix Mouse Genome 430A 2.0 gene expression chip.

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