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Gene expression profiling of macrophages: Implications for an immunosuppressive effect of dissolucytotic gold ions

ABSTRACT: Gold salts has been used in the treatment of rheumatoid arthritis but has been replaced by biologicals such as TNF-alpha inhibitors. The mechanisms behind the anti-inflammatory effect of metallic gold ions are still unknown, however, recent data showed that charged gold atoms are released from pure metallic gold implants by macrophages via a dissolucytosis membrane, and that gold ions are taken up by local macrophages, mast cells and to some extent fibroblasts. These current findings offer new treatment options for metallic gold and deeper understanding of the effect of metallic gold on key inflammatory cells as macrophages are essential. In the present study the impact of phagocytised gold ions on the global gene expression profile of the human monocytic cell line THP-1 was investigated, using microarray analysis comprising approximately 20,000 genes. The gene expression data was confirmed by measurement of three secreted proteins. A unique gene expression signature of dissolucytotic macrophages that had taken up gold ions was demonstrated. A large number of regulated genes were functionally related to immunomodulation/protection. Gold ion uptake into macrophages induced downregulation of central inflammatory cytokines as TNF-alpha, IL-32 and CD28. The data obtained in this study offer new insights into the mode of action of gold ions and suggest a future role of metallic gold as implants or topical applications in treating inflammation.

ORGANISM(S): Homo sapiens

PROVIDER: GSE37814 | GEO | 2012/12/31

SECONDARY ACCESSION(S): PRJNA163607

REPOSITORIES: GEO

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Gene expression profiling of macrophages: Implications for an immunosuppressive effect of dissolucytotic gold ions

Project description:Gold salts has been used in the treatment of rheumatoid arthritis but has been replaced by biologicals such as TNF-alpha inhibitors. The mechanisms behind the anti-inflammatory effect of metallic gold ions are still unknown, however, recent data showed that charged gold atoms are released from pure metallic gold implants by macrophages via a dissolucytosis membrane, and that gold ions are taken up by local macrophages, mast cells and to some extent fibroblasts. These current findings offer new treatment options for metallic gold and deeper understanding of the effect of metallic gold on key inflammatory cells as macrophages are essential. In the present study the impact of phagocytised gold ions on the global gene expression profile of the human monocytic cell line THP-1 was investigated, using microarray analysis comprising approximately 20,000 genes. The gene expression data was confirmed by measurement of three secreted proteins. A unique gene expression signature of dissolucytotic macrophages that had taken up gold ions was demonstrated. A large number of regulated genes were functionally related to immunomodulation/protection. Gold ion uptake into macrophages induced downregulation of central inflammatory cytokines as TNF-alpha, IL-32 and CD28. The data obtained in this study offer new insights into the mode of action of gold ions and suggest a future role of metallic gold as implants or topical applications in treating inflammation. To determine the effect of gold phagocytosis on global gene expression

2012-12-31 | E-GEOD-37814 | biostudies-arrayexpress

Data in support of Gold micro-particles for knee osteoarthritisGold micro-particles for knee osteoarthritis

Project description:This study investigated the effect of intraarticular gold micro particle implants for the treatment of pain and inflammation in KOA. The present open, exploratory, proof-of-concept study investigated whether intraarticular gold ions could act as a KOA treatment option through modulation of inflammatory mediators, pain sensitivity, and central pain mechanisms. The primary aim of this study were 1) to measure the effect on pain and function after intra-articular injection of 20 mg gold microparticles > 20 µm into the KOA joint using the patient’s synovial fluid (SF) as a carrier and 2) measure associated possible proteomic changes in the SF and serum.

2022-12-03 | PXD030746 | Pride

Gene expression profiles in human malignant melanoma cell lines exposed to carbon ions or X-rays

Project description:Little is known about molecular mechanism for its effectiveness of C-ions in melanomas. In this study, we examined the cytotoxic effects of C-ions on 6 human malignant melanoma cell lines, and gene expression profiles and cell cycle progression were also examined to reveal the mechanism of the therapeutic effectiveness of C-ions. Equivalent doses of the C-ions were more effective at reducing the survival rates than X-rays, and the relative biological effectiveness (RBE) was > 2.0 in all cell lines. In unsupervised 2D clustering performed for C-ions irradiated groups at 1 h after irradiation, many of the probes were down-regulated among 6 cell lines. We identified probes, such as XKRY, ELA3A, T-STAR, SCN9A, ELA2A, CRK7, CCNA2, CROP, CYR61, SDFR1, and SMAD4 differentially responded to C-ions and X-rays among 4 cell lines. CCNA2 was down-regulated by C-ions more than X-rays at 3 h after irradiation, and C-ions induced G2/M arrest more than X-rays in three cell lines at 30 h. Many of p53 target genes, such as ATF3, BTG2, CDKN1A, GADD45A, SESN1, and TNFRSF6 were up-regulated by C-ions at 3 h. The expressions of p53 target genes were not changed in HMV-I and MeWo. In MeWo, APG3L, RPL26 and PCNA were down-regulated or E2F2 and LIMS3 were up-regulated, and in HMV-I, ATF3, FOS, and CYR61 were up-regulated at 1 h after C-ions. In conclusion, C-ions affected p53-dependent and p53-independent pathways of cell death and cell cycle. Individual mechanism in activating of cell death was observed in each cell line of 6 melanomas. Keywords: Specific gene expression prfiles after carbon ion irradiation

2008-06-01 | GSE6630 | GEO

Potential toxicity of inorganic ions in the particulate matter: ion permeation in lung and disruption of cell metabolism

Project description:Exposure to ambient particulate matter (PM) is associated with adverse health effects. Yet, due to the complexity of its chemical composition, the molecular effects of PM exposure and the mechanism of PM-mediated toxicity remain largely unknown. Here, we show that water-soluble inorganics such as nitrate and sulfate ions, rather than PM themselves, are responsible for perturbing gene expression in the lungs by rapidly penetrating the lung surfactant barrier to the alveolar region. Furthermore, from high-throughput sequencing of lung adenocarcinoma cells, we find that exposure to nitrate and sulfate ions activates the cholesterol biosynthetic metabolism and induces the expression of genes related to tumorigenesis and inflammatory response, particularly interferon-gamma. Transcriptome analysis of mouse lungs exposed to nitrate/sulfate aerosols further supports our findings. Notably, we find that exposure to nitrate/sulfate mixture leads to a unique gene expression pattern that is not observed when nitrate or sulfate is treated alone. Our work suggests the water-soluble ions as a potential source of PM-mediated toxicity and provides a roadmap to unveil the working mechanism of health hazards of PM exposure.

2023-11-01 | GSE182629 | GEO

Homo sapiens

Project description:Gene expression profiling of macrophages: Implications for an immunosuppressive effect of dissolucytotic gold ions

| PRJNA163607 | ENA

IKKβ binds NLRP3 providing a shortcut to inflammasome activation for rapid immune responses

Project description:Quantitative proteomic profiling of TPCA-1-treated bone marrow-derived macrophages stimulated with TNF-α (50 ng/mL) for 24 h. TNF-α was used as an endogenous pro-inflammatory stimulus and inducer of sterile inflammation.

2023-03-11 | PXD036118 | Pride

Multi-omics approaches reveal TNF-mediated inhibition of tissue reparative macrophages is via a gene-selective transcriptional mechanism

Project description:Anti-TNF therapies are a core anti-inflammatory approach for chronic diseases such as rheumatoid arthritis and Crohn’s Disease. Previously, we and others found that TNF blocks the emergence and function of alternatively-activated or M2 macrophages involved in wound healing and tissue-reparative functions. Conceivably, anti-TNF drugs could mediate their protective effects in part by an altered balanced of macrophage activity. To understand the mechanistic basis of how TNF regulates tissue-reparative macrophages we used RNAseq, scRNAseq, ATACseq, time-resolved phospho-proteomics, gene-specific approaches, metabolic analysis and signaling pathway deconvolution. Our findings reveal that TNF controls tissue-reparative macrophage gene expression in a highly gene-specific way dependent on JNK signaling. We uncover principles of the selectively inhibition by TNF via the type 1 TNF receptor on specific populations of alternative activated macrophages.

2022-01-07 | PXD028667 | Pride

Copper ions inhibit Streptococcus mutans-Veillonella parvula dual biofilm by activating Streptococcus-mutans reactive nitrogen species

Project description:To investigate the inhibition mechanism of copper ions on S. mutans-V. parvula dual biofilm.

2023-02-01 | GSE222218 | GEO

Modulation of the TNF-induced macrophage response by synovial fibroblasts

Project description:Here we explored how the human macrophage response to tumor necrosis factor (TNF) is regulated by human synovial fibroblasts, the representative stromal cell type in the synovial lining of joints that become activated during inflammatory arthritis. Genome-wide transcriptome analysis (RNAseq) showed that co-cultured synovial fibroblasts modulate the expression of approximately one third of TNF-inducible genes in macrophages, including expression of target genes in pathways important for macrophage survival and polarization towards an alternatively activated phenotype. This work furthers our understanding of the interplay between innate immune and stromal cells during an inflammatory response, one that is particularly relevant to inflammatory arthritis. Our findings also identify modulation of macrophage phenotype as a new function for synovial fibroblasts that may prove to be a contributing factor in arthritis pathogenesis. Human CD14+ MCSF-differentiated macrophages were cultured with or without synovial fibroblasts in transwell chambers. TNF was added at Day 0, macrophages were harvested at Day 2. Total of 4 samples: (1) macrophages alone (2) macrophages with fibroblasts (3) macrophages with TNF (4) macrophages with fibroblasts and TNF. Macrophage RNA was purified using RNeasy mini kit (Qiagen). Tru-seq sample preparation kits (Illumina) were used to purify poly-A transcripts and generate libraries with multiplexed barcode adaptors. All samples passed quality control on a Bioanalyzer 2100 (Agilent). Paired-end reads (50 x 2 cycles, ~75x106 reads per sample) were obtained on an Illumina HiSeq 2500. The TopHat program was used to align the reads to the UCSC Hg19 human reference genome, while the Cufflinks program allowed for measurements of transcript abundance (represented by Fragments Per Kilobase of exon model per Million mapped reads (FPKM)).

2014-08-04 | E-GEOD-57723 | biostudies-arrayexpress

Response of human lymphoblastoid cells to HZE (iron ions) or gamma-rays

Project description:Transcriptional profiling of human lymphoblastoid TK6 cells comparing mock irradiated cells with cells exposed 24 hours previously to 1.67 Gy HZE (1 GeV/amu iron ions accelerated at the NASA Space Research Laboratory (NSRL) of Brookhaven National Laboratory) or 2.5 Gy 137Cs gamma rays.

2011-04-01 | GSE16518 | GEO

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