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Control of LPS induced gene expression in bone marrow derived macrophages by the p50/p105 subunit of NF-kB and IL-10

ABSTRACT: Bone marrow-derived macrophages were produced from mice lacking IL-10 alone (IL10-def) or mice lacking both IL-10 and the p50/p105 subunit of NF-kB (p50/IL10), and left unstimulated, stimulated with LPS (1 ng/ml) or stimulated with LPS and IL-10 (0.3 ng/ml). There are 12 total samples, with 2 each from the groups described in the summary. Pairwise comparisons between groups were evaluated.

ORGANISM(S): Mus musculus

SUBMITTER: Bruce Horwitz

PROVIDER: E-GEOD-19941 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Control of LPS induced gene expression in bone marrow derived macrophages by the p50/p105 subunit of NF-kB and IL-10

Project description:Bone marrow-derived macrophages were produced from mice lacking IL-10 alone (IL10-def) or mice lacking both IL-10 and the p50/p105 subunit of NF-kB (p50/IL10), and left unstimulated, stimulated with LPS (1 ng/ml) or stimulated with LPS and IL-10 (0.3 ng/ml).

2011-01-10 | GSE19941 | GEO

The specifcity of innate immune response is enforced by repression of interferon-response elements by NFkB p50

Project description:The specific binding of transcription factors to cognate sequence elements is thought to be critical for the generation of specific gene expression programs. The transcription factors nuclear factor kB (NF-kB) and the interferon (IFN) regulatory factors (IRFs) bind to the kB site and the interferon response element (IRE), respectively, of target genes, and they are activated in macrophages after exposure to pathogens. However, how these factors produce pathogen-specific inflammatory and immune responses remains poorly understood. Combining top-down and bottom-up systems biology approaches, we have identified the NF-kB p50 homodimer (p50:p50) as a regulator of IRF responses. First, unbiased genome-wide expression analysis revealed that p50 repressed a subset of IFN-inducible genes through a previously uncharacterized subclass of guanine-rich IRE (G-IRE) sequences, which was substantiated by biochemical and structural analyses. Second, mathematical modeling predicted that p50:p50 might enforce the stimulus-specificity of composite promoters. Indeed, the production of the antiviral regulator IFN-b was rendered stimulus-specific by the binding of p50:p50 to the G-IRE–containing IFNb enhancer to suppress cytotoxic IFN signaling. Specifically, a deficiency in p50 resulted in the inappropriate production of IFN-b in response to bacterial DNA sensed by Toll-like receptor 9. This role for NF-kB p50 in enforcing the specificity of the cellular response to pathogens by binding to a previously uncharacterized subset of IRE sequences alters our understanding of how the NF-kB and IRF signaling systems cooperate to regulate antimicrobial immunity. [BMDM]: Total RNA extracted from wt, p50-/- or ifnar-/- bone marrow derived macrophages (BMDMs) were subjected to stimulation with LPS, CpG or IFNb [MEF]: Total RNA extracted from wt or p50KO primary mouse embryonic fibroblasts were subjected to stimulation with LPS or IFNb

2011-03-01 | E-GEOD-27112 | biostudies-arrayexpress

Phagosome proteome of activated murine macrophage

Project description:Proteomics of carboxylated polystyrene bead (1.0 um) phagosomes from murine bone marrow-derived macrophages. cells were either resting or treated with 100 U/ml IFN-γ (PeproTech) and 100 ng/ml LPS (Sigma) for 24 h, 20 ng/ml Interleukin-4 (IL4) (BD Pharmingen) for 48 h, 20 ng/ml Interleukin-13 (IL13), 10 ng/ml Interleukin-10 (IL10)for 48 h or Reprogrammed (IL4 was incubated with BMDMs for 24 h, and the medium was replaced with fresh medium containing IFN-γ/LPS to incubate for another 24 h). Phagosomes were isolated after 30 min bead inoculation.

2019-03-22 | PXD004520 | Pride

The regulatory roles of Ezh2 in response to lipopolysaccharide (LPS) in macrophages and mice with conditional Ezh2 deletion with LysM-Cre system

Project description:The responses of macrophages to lipopolysaccharide (LPS) might determine the direction of clinical manifestations of sepsis, which is the immune response against severe infection. Meanwhile, the enhancer of zeste homologue 2 (Ezh2), a histone lysine methyltransferase of epigenetic regulation, might interfere with LPS response. With a single LPS stimulation, Ezh2 null(Ezh2flox/flox; LysM-Crecre/−) macrophages demonstrated lower supernatant TNF-α than Ezh2 control (Ezh2fl/fl; LysM-Cre−/−), perhaps due to an upregulation of Socs3, which is a suppressor of cytokine signaling 3, due to the loss of the Ezh2 gene. In LPS tolerance, Ezh2 null macrophages indicated higher supernatant TNF-α and IL-6 than the control, supporting an impact of the loss of the Ezh2 inhibitory gene. In parallel, Ezh2 null mice demonstrated lower serum TNF-α and IL-6 than the control mice after an LPS injection, indicating a less severe LPS-induced hyper-inflammation in Ezh2 null mice. In conclusion, an absence of Ezh2 in macrophages resulted in less severe LPS-induced inflammation, as indicated by low serum cytokines, with less severe LPS tolerance, as demonstrated by higher cytokine production, partly through the upregulated Socs3.

2023-07-20 | PXD041265 | Pride

Inflammatory mediators alter astrocyte genomic profiles and G-protein receptor evoked calcium signaling

Project description:Inflammation features in diverse central nervous system disorders such as stroke, trauma, neurodegeneration, infection and autoimmunity. To better understand how inflammatory mediators may alter astrocyte functions, we examined the effects of transforming growth factor-Î²1 (TGF-Î²1), lipopolysaccharide (LPS) and interferon-gamma (IFNÎ³) on purified, murine, primary cortical astrocyte cultures. We used microarrays to conduct whole genome expression profiling, and measured calcium signaling, which is implicated in mediating dynamic astrocyte functions. Combinatorial exposure to TGF-Î²1, LPS and IFNÎ³ significantly modulated astrocyte expression of over 6,800 genes and resulted in both additive and synergistic changes compared with individual stimuli alone. Bioinformatic analysis revealed that combinatorial treatment significantly and markedly up regulated molecular networks and pathways associated with immune signaling and with regulation of cell compromise, death, growth and proliferation. These findings provide databases of astrocyte transcriptome changes elicited by the inflammatory stimuli, TGF-Î²1, LPS and IFNÎ³ alone and in combination, and show that these stimuli up regulate astrocyte molecular networks associated with immune- and injury-related functions and significantly alter astrocyte calcium signaling evoked by multiple GPCR. We used microarrays to examine the effects of transforming growth factor-Î²1 (TGF-Î²1), lipopolysaccharide (LPS) and interferon-gamma (IFNÎ³) on purified, murine, primary cortical astrocyte cultures.

2012-10-18 | E-GEOD-36089 | biostudies-arrayexpress

Transcription profiling of mouse bone marrow macrophages from IL-6-/- and IL-10-/- mutants treated with IL-10 or IL-6 stimulation in the presence of LPS

Project description:IL-10 or IL-6 stimulation of control 129xC57BL/6 murine bone marrow derived macrophages in the presence of LPS. We used microarrays to detail the global programme of gene expression changes in response to IL-6 or IL-10 stimulation in the presence of lipopolysaccharide. BMDMs were isolated from control, IL-6-/-, and IL-10-/- mice on a 129XBL/6 mixed background mice and differentiated in the presence of CSF-1 for 6-7 days. Cells were scraped and plated in 6 well plates at 2x10e6/well. Cells were washed with complete DMEM and rested for 1-2 hr before stimulation with combinations of IL-10 (10 ng/ml), IL-6 (2 ng/ml) or LPS (100 ng/ml) for 45 min or 180 mins. Complete biological replicates were performed. Experiment Overall Design: Data sets from wild-type, IL-10-/- and IL-6-/- BMDMs treated with IL-6 or IL-10 in the presence of LPS over time

2008-06-13 | E-GEOD-5589 | biostudies-arrayexpress

Transcription profiling by array of mouse intestinal epithelial m-ICcl2 cells stimulated with lipopolysaccharide

Project description:m-ICcl2 cells (Bens et al., Am. J. Physiol., 1996) were grown for 6 days on collagen coated cell culture flasks in medium as recommended (see ference above). Medium was changed every 48 hours. The cells were mycoplasma tested (PCR) and found negative. The medium and PBS was endotoxin tested (ELISA) and found to be negative (< 50pg/mL). Unstimulated cells (control) were left cultured in medium only. Lipopolysaccharide (100 ng/mL in water, D31m4 E. coli LPS from List Biochemicals) was sonicated (10 min_ prior to use. Cells were stimulated 6 hours with 100 ng/mL LPS and harvested or stimulated with LPS (100 ng/mL) and washed with warm phosphate buffered saline (PBS) after 6 hours, followed by medium change every 48 hours. Cells were harvested after 96 hours (6 hours incubated in the presence of LPS, 90 hours after stimulation). RNA was isolated after repeated (3x) washing with PBS using Trizol reagent (1 mL/75 cm2) using the standard protocol and resuspended in Millipore water. Quantification was done by spectroscopy and the RNA was stored at -80C.

2011-08-26 | E-MTAB-355 | biostudies-arrayexpress

Transcription profiling of mouse cell culture treated with LPS to identify of inflammatory genes suppressed by heat shock

Project description:To clarify inflammatory genes whose expression is suppressed at high temperatures, we performed comprehensive analysis of gene expression by using a DNA microarray. Two independent primary cultures of mouse embryo fibroblasts (MEF1 and MEF2) were treated with LPS for 4 hours, or treated with LPS for 4 hours after the pretreatment with heat shock at 42ËC for 1 hour, and we identified 100 genes that undergo more than a 3-fold increase with LPS treatment. Remarkably, 86 genes (86%) underwent less than a 2-fold increase after combined treatments with heat shock and LPS in MEF1 and MEF2 cells. Experiment Overall Design: Total RNAs were prepared from two primary cultures of mouse embryo fibroblasts (MEF) derived from two independent embryos at embryonic day 15.5 (ICR mice). Cells were maintained at 37ËC (Control), treated with lipopolysaccharide (LPS, E. coli 0127:B8, Sigma, 1 Î¼g/ml) for 4 hours, or treated with LPS for 4 hours after the pretreatment of heat shock at 42ËC for 1 hour. Gene expression was analyzed by using GeneChip Mouse Genome 430 2.0 Array (Affymetrix, Santa Clara, CA).

2010-01-19 | E-GEOD-16266 | biostudies-arrayexpress

Investigsting the role of NF-ĸB p50 S80 phosphorylation in regulating LPS-induced transcription in THP-1 cells

Project description:Phosphorylation of the NF-ĸB p50 subunit is known to regulate target gene expression. The role of p50 S80 phosphorylation in regulating LPS-induced transcription by utilising wild type (WT) and NFKB1S80A THP-1 cells is investigated.

2020-09-19 | GSE120212 | GEO

Transcription profiling of human macrophages treated with lipopolysaccharide plus INF-g, IL-10 or rhAPC

Project description:Macrophages treated with INF-g (100 U/ml)and LPS (10 ng/ml), or INF-g (100 U/ml), LPS (10 ng/ml)and IL-10 (5 ng/mL), or INF-g (100 U/ml), LPS (10 ng/ml)and rhAPC(5 ug/mL. Each treatment is hybridized against untreated macrophages

2007-09-27 | E-MEXP-927 | biostudies-arrayexpress

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