Transcriptomics of THP-1 macrophages after treatment with NLRP3-induced EVs
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ABSTRACT:
PROVIDER: PRJNA749268 | ENA |
REPOSITORIES: ENA
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Project description:Inflammasome activation in macrophages induces the release of EVs, however, the effect of these inflammasome-induced EVs on recipient cells is poorly characterized. To characterize the effect EVs released upon LPS + nigericin stimulation, we performed 3' sequencing on the recipient cells (NLRP3 KO THP-1 macrophages and NLRP3 KO THP-1 macrophages that have been reconstituted with NLRP3 to resemble the WT). As controls, RNA isolated from EVs themselves or LPS- or nigericin-treated cells were subjected to 3' sequencing.
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Project description:Inflammasome-activated cells undergo an inflammatory cell death associated with the release of potent pro-inflammatory cytokines and poorly characterized extracellular vesicles (EVs). Since inflammasome-induced EVs could signal inflammasome pathway activation in patients with chronic inflammation and modulate bystander cell activation, we performed a systems analysis of the RNA content and function of two EV classes. Therefore, PMA-differentiated THP-1 macrophages were either stimulated with inflammasome activators or TLR ligands and subsequently differently sized EVs (10K and SEC EVs) were isolated from the tissue culture supernatant. The RNA contained within EV preparations was extracted and subjected to the Clariom D microarray. Web link to Clariom D chip: https://www.thermofisher.com/order/catalog/product/902925?de&en#/902925?de&en
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Project description:THP-1 macrophages were treated with EVs and stimulated with LPS, and then total RNA was extracted from cells. Extracted total RNAs were investigated by microarray analysis. Increase and decrease of mRNA expression were investigated between EV-treated and non-treated THP-1 macrophages.
2020-03-01 | GSE127714 | GEO
Project description:Inflammasome, activated by pathogen-derived and host-derived danger signals, constitutes a multimolecular signaling complex that serves as a platform for caspase-1 (CASP1) activation and interleukin-1beta (IL1B) maturation. The activation of NLRP3 inflammasome requires two-step signals. The first “priming” signal (Signal 1) enhances gene expression of inflammasome components. The second “activation” signal (Signal 2) promotes the assembly of inflammasome components. Deregulated activation of NLRP3 inflammasome contributes to the pathological processes of Alzheimer’s disease (AD) and multiple sclerosis (MS). However, at present, the precise mechanism regulating NLRP3 inflammasome activation and deactivation remains largely unknown. By genome-wide gene expression profiling, we studied the molecular network of NLRP3 inflammasome activation-responsive genes in a human monocyte cell line THP-1 sequentially given two-step signals. We identified the set of 83 NLRP3 inflammasome activation-responsive genes. Among them, we found the NR4A nuclear receptor family NR4A1, NR4A2, and NR4A3, the EGR family EGR1, EGR2, and EGR3, the IkappaB family NFKBIZ, NFKBID, and NFKBIA as a key group of the genes that possibly constitute a negative feedback loop for shutting down inflammation following NLRP3 inflammasome activation. By molecular network analysis, we identified a complex network of NLRP3 inflammasome activation-responsive genes involved in cellular development and death, and immune and inflammatory responses, where transcription factors AP-1, NR4A, and EGR serve as a hub. Thus, NLRP3 inflammasome activation-responsive genes constitute the molecular network composed of a set of negative feedback regulators for prompt resolution of inflammation. To load the Signal 1 (S1), THP-1 cells were incubated for 3 hours in the culture medium with or without inclusion of 0.2 microgram/ml lipopolysaccharide (LPS). To load the Signal 2 (S2), they were incubated further for 2 hours in the culture medium with inclusion of 10 microM nigericin sodium salt dissolved in ethanol or the equal v/v% concentration of ethanol (vehicle), followed by processing for microarray analysis on Human Gene 1.0 ST Array (Affymetrix).
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Project description:Viral antigens can activate phagocytes inducing inflammation but the mechanisms are barely explored. This study aimed to investigate the capability of viral oligomeric proteins of different structure to induce inflammatory response in macrophages. Human THP-1 cell line was used to prepare macrophages which were treated with filamentous nucleocapsid-like particles (NLPs) of paramyxoviruses and spherical virus-like particles (VLPs) of human polyomaviruses. The effects of viral proteins on cell viability, pro-inflammatory cytokines’ production and formation of NLRP3 inflammasome components, ASC specks, were investigated. Filamentous NLPs did not induce inflammation markers while spherical VLPs mediated inflammatory response followed by NLRP3 inflammasome activation. Inhibitors of cathepsins and K+ efflux decreased IL-1β levels and cell death indicating a complex inflammasome activation process. Similar activation pattern was observed in primary human macrophages treated with VLPs. Single cell RNAseq analysis of THP-1 cells revealed several cell activation states characterized by high expression of inflammation-related genes. This study provides new insights into interaction of viral proteins with innate immune cells and suggests that structural properties of oligomeric proteins may define cell activation pathways.
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Project description:The effect of SAA1 treatment on global gene expression in THP-1 macrophages was studied. The study determined the gene expression upon wild-type SAA1 treatment, variant SAA1 treatment (p.Gly72Asp) and in untreated THP-1 macrophages. SAA1 treatment of macrophages induces the expression of genes involved in inflammation, angiogenesis, phagocytosis and tissue remodeling which are important in the pathogenesis of chronic inflammatory diseases such as atherosclerosis and rheumatoid arthritis. THP-1 macrophages were treated with SAA1 for either 8 hours or 24 hours. RNA were then extracted and the gene expression pattern was compared between (i) wild-type SAA1 vs untreated (ii) variant SAA1 vs wild-type SAA1 at both 8 hr and 24 hr.
2011-05-11 | E-GEOD-28785 | biostudies-arrayexpress
Project description:Purpose: The aim of this study was to obtain a comprehensive transcriptomic analysis of IL-26-exposed macrophages. Methods: THP-1 derived macrophage were generated by incubating THP-1 cells with PMA (50 ng/ml) for 24h.Then THP-1 macrophages were treated with IL-26 for 24h, which were collected and applied to RNA-sequencing. The constructed sequencing library was sequenced using an Illumina Novaseq 6000 system. The expression of transcripts was calculated as fragments per kilobase of exon model per million mapped reads (FPKM). Results: In total, we identified 1303 differentially expressed protein-coding genes between untreated and IL-26-treated macrophages, including 667 up-regulated and 636 down-regulated genes.
2022-04-27 | GSE192493 | GEO
Project description:Inflammasome, activated by pathogen-derived and host-derived danger signals, constitutes a multimolecular signaling complex that serves as a platform for caspase-1 (CASP1) activation and interleukin-1beta (IL1B) maturation. The activation of NLRP3 inflammasome requires two-step signals. The first “priming” signal (Signal 1) enhances gene expression of inflammasome components. The second “activation” signal (Signal 2) promotes the assembly of inflammasome components. Deregulated activation of NLRP3 inflammasome contributes to the pathological processes of Alzheimer’s disease (AD) and multiple sclerosis (MS). However, at present, the precise mechanism regulating NLRP3 inflammasome activation and deactivation remains largely unknown. By genome-wide gene expression profiling, we studied the molecular network of NLRP3 inflammasome activation-responsive genes in a human monocyte cell line THP-1 sequentially given two-step signals. We identified the set of 83 NLRP3 inflammasome activation-responsive genes. Among them, we found the NR4A nuclear receptor family NR4A1, NR4A2, and NR4A3, the EGR family EGR1, EGR2, and EGR3, the IkappaB family NFKBIZ, NFKBID, and NFKBIA as a key group of the genes that possibly constitute a negative feedback loop for shutting down inflammation following NLRP3 inflammasome activation. By molecular network analysis, we identified a complex network of NLRP3 inflammasome activation-responsive genes involved in cellular development and death, and immune and inflammatory responses, where transcription factors AP-1, NR4A, and EGR serve as a hub. Thus, NLRP3 inflammasome activation-responsive genes constitute the molecular network composed of a set of negative feedback regulators for prompt resolution of inflammation.
2014-07-01 | GSE58959 | GEO
Project description:The effect of SAA1 treatment on global gene expression in THP-1 macrophages was studied. The study determined the gene expression upon wild-type SAA1 treatment, variant SAA1 treatment (p.Gly72Asp) and in untreated THP-1 macrophages. SAA1 treatment of macrophages induces the expression of genes involved in inflammation, angiogenesis, phagocytosis and tissue remodeling which are important in the pathogenesis of chronic inflammatory diseases such as atherosclerosis and rheumatoid arthritis.
2011-05-11 | GSE28785 | GEO