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Gene expression data from yerba mate treated and non-treated cultured PBMCs activated with phytohemagglutinin

ABSTRACT: Yerba mate (YM) has been shown to have anti-inflammatory properties in several studies. However, this effect has been found mainly in obesity-related in inflammation. The aim of this work was to study the effect of YM in cultured peripheral blood mononuclear cells to see whether it has anti-inflammatory properties. We stimulated peripheral blood mononuclear cells in vitro with phitohemaglutinin in the presence of yerba mate and determined their activation measuring the the expression of CD25 by flow cytometry. We observed that YM treatment produced a dose-dependent reduction in PBMC activation (CD25 positive cells) when they were stimulated with PHA. This effect was also observed in T cells (CD3 positive) subpopulation. Microarray analysis revealed the differential expression of 128 genes in YM-treated cells. According to a protein-protein interaction database, these genes were highly connected and they are involved in inflammatory response. In summary, it was demonstrated that YM produces a reduction in the amount of activated cells under the stimulation of PHA. Therefore, it might be used in diseases with an inflammatory component. PBMC samples from a healthy individual were cultured and stimulated with phytohemagglutinin. Gene expression of yerba mate treated and non-treated cells was analyzed in duplicates, having in total four microarrays.

ORGANISM(S): Homo sapiens

SUBMITTER: Maider MuÃ±oz-Culla

PROVIDER: E-GEOD-84407 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Gene expression data from yerba mate treated and non-treated cultured PBMCs activated with phytohemagglutinin

Project description:Yerba mate (YM) has been shown to have anti-inflammatory properties in several studies. However, this effect has been found mainly in obesity-related in inflammation. The aim of this work was to study the effect of YM in cultured peripheral blood mononuclear cells to see whether it has anti-inflammatory properties. We stimulated peripheral blood mononuclear cells in vitro with phitohemaglutinin in the presence of yerba mate and determined their activation measuring the the expression of CD25 by flow cytometry. We observed that YM treatment produced a dose-dependent reduction in PBMC activation (CD25 positive cells) when they were stimulated with PHA. This effect was also observed in T cells (CD3 positive) subpopulation. Microarray analysis revealed the differential expression of 128 genes in YM-treated cells. According to a protein-protein interaction database, these genes were highly connected and they are involved in inflammatory response. In summary, it was demonstrated that YM produces a reduction in the amount of activated cells under the stimulation of PHA. Therefore, it might be used in diseases with an inflammatory component.

2016-08-15 | GSE84407 | GEO

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Transcription profiling of human PBMC treated with anti-CD25 mAb

Project description:CD25 monoclonal antibody binding to the alpha-chain of the Interleukin-2 (IL-2) receptor, blocks high affinity IL-2 binding thereby preventing complete T cell activation and being of ample importance in transplantation medicine and potentially the treatment of autoimmune disease. However, CD25 antibodies do not only block T cell activation but also prevent activation induced cell death (AICD) attributing a dual function to IL-2. In this study, the modulation of the genomic expression profile of human peripheral blood mononuclear cells (PBMC) with therapeutic concentrations of humanized anti-CD25 mAb was investigated. PBMC were stimulated with CD3 antibody OKT-3 together with recombinant IL-2 in the absence or presence of anti-CD25 mAb. RNA was extracted and subjected to microarray analysis on U133A microarrays (Affymetrix). The expression profile revealed the up-regulation of 62 genes and down-regulation of 38 genes by anti-CD25 mAb, respectively. Experiment Overall Design: Peripheral blood mononuclear cells (PBMC) were stimulated for 8 or 16 hrs with 100 ng/ml OKT-3 together with 100 U/ml recombinant human interleukin-2 (rhIL-2) in the absence or presence of 30 Âµg/ml anti-CD25 antibody. RNA from cells under such treatment was isolated with Trizol and subjected to microarray analysis onto human U133A microarray following the Affymetrix protocol.

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Expression data from healthy control human peripheral blood mononuclear cells (PBMC) treated with wild-type IL-2 or F42K

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2016-09-01 | E-GEOD-77601 | biostudies-arrayexpress

Influence of anti-CD25 mAb on the transcriptome of activated PBMC

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2022-10-31 | E-MTAB-12197 | biostudies-arrayexpress

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2012-09-01 | E-GEOD-35716 | biostudies-arrayexpress

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Project description:Purpose: We analyzed RNA-seq from peripheral blood mononuclear cells (PBMC) in DMARDs-naïve RA patients and healthy subjects. Our goal was to evaluate the transcriptional profiles of ST2825-treated PBMC to identify its therapeutic potential. Methods: We analyzed bulk RNA-seq from peripheral blood mononuclear cells (PBMC) in DMARDs-naïve RA patients after stimulation with LPS and IL-1β, PBMC were treated with the MyD88 chemical inhibitor, ST2825. Collection of RNA was performed after 24 h of treatment and samples were sequenced to determine transcriptional changes and regulated processes in treated PBMC. Results: paired-end reads were mapped to the hg19 human genome assembly. RNA levels were normalized using DESeq. We identified 796 differentially expressed (DE) genes by 2-fold change (p<0.05) between RA patients and healthy subjects. Our analysis revealed 631 DE genes between DMARDs-naïve RA patients before and after ST2825 treatment. We identified 471 DE genes between LPS-stimulated RA PBMC and LPS-stimulated RA PBMC treated with ST2825. Conclusion: Our study provides comprehensive evidence supporting the potential application of the MyD88 inhibitor, ST2825, as a modulator of gene expression signtaures involved in pathogenic processes in PBMC from DMARDs-naïve RA patients. Our indepth analysis of RNA-seq data will serve as a valuable resource containing the inflammatory gene expression signatures by MyD88.

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