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Age-associated Changes in Basal NF-κB Function in Human CD4+ T Lymphocytes via Dysregulation of PI3 Kinase (dataset 2)

ABSTRACT: Immune impairment and high circulating level of pro-inflammatory cytokines are landmarks of human aging. However, the molecular basis of immune dysregulation and the source of inflammatory markers remain unclear. Here we demonstrate that in the absence of overt cell stimulation, gene expression mediated by the transcription factor NF-κB is higher in purified and rested human CD4+ T lymphocytes from older compared to younger individuals. This increase of NF-κB -associated transcription includes transcripts for pro-inflammatory cytokines such as IL-1 and chemokines such as CCL2 and CXCL10. We demonstrate that NF-κB up-regulation is cell-intrinsic and mediated in part by phosphatidylinositol 3-kinase (PI3K) activity induced in response to metabolic activity, which can be moderated by rapamycin treatment. Our observations provide direct evidence that dysregulated basal NF-κB activity may contribute to the mild pro-inflammatory state of aging.

ORGANISM(S): Homo sapiens

PROVIDER: GSE62332 | GEO | 2015/01/08

SECONDARY ACCESSION(S): PRJNA263936

REPOSITORIES: GEO

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Project description:Immune impairment and high circulating level of pro-inflammatory cytokines are landmarks of human aging. However, the molecular basis of immune dysregulation and the source of inflammatory markers remain unclear. Here we demonstrate that in the absence of overt cell stimulation, gene expression mediated by the transcription factor NF-ÎºB is higher in purified and rested human CD4+ T lymphocytes from older compared to younger individuals. This increase of NF-ÎºB -associated transcription includes transcripts for pro-inflammatory cytokines such as IL-1 and chemokines such as CCL2 and CXCL10. We demonstrate that NF-ÎºB up-regulation is cell-intrinsic and mediated in part by phosphatidylinositol 3-kinase (PI3K) activity induced in response to metabolic activity, which can be moderated by rapamycin treatment. Our observations provide direct evidence that dysregulated basal NF-ÎºB activity may contribute to the mild pro-inflammatory state of aging. Peripheral blood mononuclear cells (PBMCs) were isolated from heparinized blood using Ficoll-Paque Plus density gradient centrifugation. CD4+ T cells were obtained by positive selection using anti-human CD4 microbeads. After incubation for 4hr at either 4 or 37 Degrees C, cells were harvested and collected by centrifugation. Total cellular RNA was prepared using Qiagen RNeasy protocols. Labeling and amplification were done with the standard Illumina protocol and the biotin-labeled cRNA was hybridized to Illumina's HumanHT-12 V3.0 Expression BeadChip. The arrays were washed, blocked and the biotin-labeled cRNA was detected by staining with streptavidin-Cy3.

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Project description:Immune impairment and high circulating level of pro-inflammatory cytokines are landmarks of human aging. However, the molecular basis of immune dysregulation and the source of inflammatory markers remain unclear. Here we demonstrate that in the absence of overt cell stimulation, gene expression mediated by the transcription factor NF-ÎºB is higher in purified and rested human CD4+ T lymphocytes from older compared to younger individuals. This increase of NF-ÎºB -associated transcription includes transcripts for pro-inflammatory cytokines such as IL-1 and chemokines such as CCL2 and CXCL10. We demonstrate that NF-ÎºB up-regulation is cell-intrinsic and mediated in part by phosphatidylinositol 3-kinase (PI3K) activity induced in response to metabolic activity, which can be moderated by rapamycin treatment. Our observations provide direct evidence that dysregulated basal NF-ÎºB activity may contribute to the mild pro-inflammatory state of aging. Peripheral blood mononuclear cells (PBMCs) were isolated from heparinized blood using Ficoll-Paque Plus density gradient centrifugation. CD4+ T cells were obtained by positive selection using anti-human CD4 microbeads. After a 4h incubation at 37ÂºC (5% CO2 incubator), cells were harvested and collected by centrifugation. Total cellular RNA was prepared using Qiagen RNeasy protocols. Labeling and amplification were done with the standard Illumina protocol, and the biotin-labeled cRNA was hybridized to Illumina's HumanRef-8 v2.0 Expression BeadChip. The arrays were washed, blocked and the biotin-labeled cRNA was detected by staining with streptavidin-Cy3. Samples were divided into 2 age groups, young and old, with the cut off at 65 years and above as old.

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Project description:Immune impairment and high circulating level of pro-inflammatory cytokines are landmarks of human aging. However, the molecular basis of immune dysregulation and the source of inflammatory markers remain unclear. Here we demonstrate that in the absence of overt cell stimulation, gene expression mediated by the transcription factor NF-ÎºB is higher in purified and rested human CD4+ T lymphocytes from older compared to younger individuals. This increase of NF-ÎºB -associated transcription includes transcripts for pro-inflammatory cytokines such as IL-1 and chemokines such as CCL2 and CXCL10. We demonstrate that NF-ÎºB up-regulation is cell-intrinsic and mediated in part by phosphatidylinositol 3-kinase (PI3K) activity induced in response to metabolic activity, which can be moderated by rapamycin treatment. Our observations provide direct evidence that dysregulated basal NF-ÎºB activity may contribute to the mild pro-inflammatory state of aging. Peripheral blood mononuclear cells (PBMCs) were isolated from heparinized blood using Ficoll-Paque Plus density gradient centrifugation. CD4+ T cells were obtained by positive selection using anti-human CD4 microbeads. After a 4h incubation at 37ÂºC (5% CO2 incubator), cells were harvested and collected by centrifugation. Total cellular RNA was prepared using Qiagen RNeasy protocols. Labeling and amplification were done with the standard Illumina protocol, and the biotin-labeled cRNA was hybridized to Illumina's HumanHT-12 v4 Expression BeadChip. The arrays were washed, blocked and the biotin-labeled cRNA was detected by staining with streptavidin-Cy3. Samples were divided into 2 age groups, young and old, with the cut off at 65 years and above as old.

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Age-associated Changes in Basal NF-ÎºB Function in Human CD4+ T Lymphocytes via Dysregulation of PI3 Kinase (dataset 4)

Project description:Immune impairment and high circulating level of pro-inflammatory cytokines are landmarks of human aging. However, the molecular basis of immune dysregulation and the source of inflammatory markers remain unclear. Here we demonstrate that in the absence of overt cell stimulation, gene expression mediated by the transcription factor NF-ÎºB is higher in purified and rested human CD4+ T lymphocytes from older compared to younger individuals. This increase of NF-ÎºB -associated transcription includes transcripts for pro-inflammatory cytokines such as IL-1 and chemokines such as CCL2 and CXCL10. We demonstrate that NF-ÎºB up-regulation is cell-intrinsic and mediated in part by phosphatidylinositol 3-kinase (PI3K) activity induced in response to metabolic activity, which can be moderated by rapamycin treatment. Our observations provide direct evidence that dysregulated basal NF-ÎºB activity may contribute to the mild pro-inflammatory state of aging. Peripheral blood mononuclear cells (PBMCs) were isolated from heparinized blood using Ficoll-Paque Plus density gradient centrifugation. CD4+ T cells were obtained by positive selection using anti-human CD4 microbeads. To test the effects of serum, 5x10^6 CD4+ T cells in 3 ml of RPMI 1640 with serum or AIM V (Life Technologies, Carlsbad, CA, USA) serum-free medium were held at 4Â°C or incubated for 4h at 37ÂºC (5% CO2 incubator). After incubation, cells were harvested and collected by centrifugation. Total cellular RNA was prepared using Qiagen RNeasy protocols. Labeling and amplification were done with the standard Illumina protocol and the biotin-labeled cRNA was hybridized to Illumina's HumanHT-12 V4.0 Expression BeadChip. The arrays were washed, blocked and the biotin-labeled cRNA was detected by staining with streptavidin-Cy3.

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Age-associated Changes in Basal NF-ÎºB Function in Human CD4+ T Lymphocytes via Dysregulation of PI3 Kinase (dataset 5)

Project description:Immune impairment and high circulating level of pro-inflammatory cytokines are landmarks of human aging. However, the molecular basis of immune dysregulation and the source of inflammatory markers remain unclear. Here we demonstrate that in the absence of overt cell stimulation, gene expression mediated by the transcription factor NF-ÎºB is higher in purified and rested human CD4+ T lymphocytes from older compared to younger individuals. This increase of NF-ÎºB -associated transcription includes transcripts for pro-inflammatory cytokines such as IL-1 and chemokines such as CCL2 and CXCL10. We demonstrate that NF-ÎºB up-regulation is cell-intrinsic and mediated in part by phosphatidylinositol 3-kinase (PI3K) activity induced in response to metabolic activity, which can be moderated by rapamycin treatment. Our observations provide direct evidence that dysregulated basal NF-ÎºB activity may contribute to the mild pro-inflammatory state of aging. Peripheral blood mononuclear cells (PBMCs) were isolated from heparinized blood using Ficoll-Paque Plus density gradient centrifugation. CD4+ T cells were obtained by positive selection using anti-human CD4 microbeads. To test the effects of drug treatment, 5x10^6 CD4+ T cells were treated with varying concentrations of rapamycin and also LY 294002 in 3 ml of RPMI 1640 medium. Control cells were also created without any added drugs. Cells were incubated for 4h in 5% CO2 at both 37Â°C and 4Â°C. After incubation, cells were harvested and collected by centrifugation. Total cellular RNA was prepared using Qiagen RNeasy protocols. Labeling and amplification were done with the standard Illumina protocol and the biotin-labeled cRNA was hybridized to Illumina's HumanHT-12 V4.0 Expression BeadChip. The arrays were washed, blocked and the biotin-labeled cRNA was detected by staining with streptavidin-Cy3.

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A pseudogene lncRNA at the interface of inflammation and anti-inflammatory therapeutics

Project description:Pseudogenes are thought to be inactive gene sequences, but recent evidence of extensive pseudogene transcription raised the question of potential function. Here we discover and characterize the sets of lncRNAs induced by inflammatory signaling via TNFα. TNFα regulates hundreds of lncRNAs, including 54 pseudogene lncRNAs, several of which show exquisitely selective expression in response to specific cytokines and microbial components in a NF-κB-dependent manner. Lethe, a pseudogene lncRNA, is selectively induced by proinflammatory cytokines via NF-κB or glucocorticoid receptor agonist, and functions in negative feedback signaling to NF-κB. Lethe interacts with NF-κB subunit RelA to inhibit RelA DNA binding and target gene activation. Lethe level decreases with organismal age, a physiological state associated with increased NF-κB activity. These findings suggest that expression of pseudogenes lncRNAs are actively regulated and constitute functional regulators of inflammatory signaling. RNA profiles of wild type (WT) MEFs treated with TNF-alpha were generated by deep sequencing using Illumina GAIIx. Examination of H3K4me3 histome modification in MEF.

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