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10x single-cell RNAseq profiling of influenza Virus infected Human PBMCs treated with Dimethyl itaconate

ABSTRACT: 10x single-cell RNAseq profiling of influenza Virus infected Human PBMCs treated with Dimethyl itaconate

PROVIDER: PRJNA692448 | ENA |

REPOSITORIES: ENA

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10x single-cell RNAseq profiling of influenza Virus infected Human PBMCs treated with Dimethyl itaconate

Project description:Itaconic acid and its variant Dimethyl itaconate (DI) have shown an anti-inflammatory effect in different human cell lines and PBMCs during Infleunza A virus (IAV) infection. In this experiment, we further explored which cell types in PBMCs respond to IAV infection and DI treatment.

2021-10-31 | GSE164922 | GEO

Expression data from PBMCs infected with influenza A virus and treated with/without Itaconate

Project description:Analysis of gene expression in human PBMCs infected with influenza A virus or Mock and treated with Itaconic acid, Dimethyl itaconate or 4-Octyl itaconate to investigate the effects itaconate have on transcriptional response in human PBMCs. We particularly looked at anti-inflammatory effects of itaconate in inflammation followed by Influenza A virus infection.

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Expression data from A549 cell line infected with influenza A virus (IAV) and treated with/without Itaconate

Project description:Analysis of gene expression in A549 cells infected with influenza A virus or Mock and treated with Itaconic acid (IA), or Dimethyl itaconate (DI) to investigate the effects itaconate have on transcriptional response in A549 cells. We particularly looked at anti-inflammatory effects of itaconate in inflammation followed by Influenza A virus infection.

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Expression data from differentiated THP-1 (dTHP-1) cell line infected with influenza A virus (IAV) and treated with/without Itaconate

Project description:Analysis of gene expression indTHP-1 cells infected with influenza A virus or Mock and treated with Itaconic acid (IA), or Dimethyl itaconate (DI) to investigate the effects itaconate have on transcriptional response in dTHP-1 cells. We particularly looked at anti-inflammatory effects of itaconate in inflammation followed by Influenza A virus infection.

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RankL induced mice BMM treated with or without dimethyl itaconate for 24h

Project description:RankL induced mice BMM following dimethyl itaconate treatment for 24h

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Dimethyl itaconate inhibits secondary wave of NF-κB signaling in macrophage activation

Project description:Natural metabolite itaconate and its membrane permeable derivative dimethyl itaconate (DI) selectively inhibit a subset of cytokines during macrophage activation (e.g. IL-1β, IL-6, IL-12 but not TNF-α). Selectivity of DI action stems from the inhibitory effects of secondary, but not primary, wave of NF-κB signaling.

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Expression data from hiPSC derived WT and ISG15 KO endothelial cells stimulated with interferon-a and treated with itaconic acid, dimethyl itaconate, 4-octyl itaconate and ruxolitinib

Project description:Analysis of gene expression in WT and ISG15 KO endothelial cells, stimulated with IFNa and treated with Itaconic acid (IA), Dimethyl itaconate (DI), 4-octyl itaconate (4OI) and ruxolitinib (RUX) to investigate the effects of treatments on transcriptional response in the cells.

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Expression data from PBMCs infected with influenza A virus and treated with/without Itaconate

Project description:Expression data from PBMCs infected with influenza A virus and treated with/without Itaconate

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Dimethyl Itaconate alleviates the pyroptosis of macrophages through oxidative stress

Project description:Macrophages are involved in the pathophysiology of many diseases as critical cells of the innate immune system. Pyroptosis is a form of macrophage death that induces cytokinesis of phagocytic substances in the macrophages, thereby defending against infection. Dimethyl itaconate (DI) is an analog of itaconic acid with anti-inflammatory effects. However, the effect of dimethyl itaconate on macrophage pyroptosis has not been elucidated clearly. Thus, the present study aimed to analyze the effect of DI treatment on a macrophage pyroptosis model (Lipopolysaccharide, LPS+Adenosine Triphosphate, ATP). The results showed that 0.25 mM DI ameliorated macrophage pyroptosis and downregulated interleukin (IL)-1β expression. Then, real-time quantitative polymerase chain reaction (RT-qPCR) was used to confirm the result of RNA-sequencing of the upregulated oxidative stress-related genes (Gclc and Gss) and downregulated inflammation-related genes (IL-12β and IL-1β). In addition, Gene Ontology (GO) enrichment analysis showed that differential genes were associated with transcript levels and DNA replication. Kyoto encyclopedia of genes and genomes (KEGG) enrichment showed that signaling pathways, such as tumor necrosis factor (TNF), Jak, Toll-like receptor and IL-17, were altered after DI treatment. N-acetyl-L-cysteine (NAC) reversed the DI effect on the LPS+ATP-induced macrophage pyroptosis and upregulated the IL-1β expression. Oxidative stress-related protein Nrf2 is involved in the DI regulation of macrophage pyroptosis. Taken together, these findings suggested that DI alleviates the pyroptosis of macrophages through oxidative stress.

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Dimethyl Itaconate alleviates the pyroptosis of macrophages through oxidative stress

Project description:Dimethyl Itaconate alleviates the pyroptosis of macrophages through oxidative stress

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