Similar Datasets
Project description:Lipid accumulation associated with immune cell infiltration leading to hepatocellular ballooning and lobular inflammation are the cardinal features of NASH. With onset and development of multi-omics approaches in the last decade, we have been able to comprehend the existence and functionality of gut microbial ecology. Apart from the compositional variation (dysbiosis), functional alteration of the microbial population i.e., the impact of the crosstalk between gut microbiota-derived metabolites with host cells also remains elusive in terms of regulation of immunometabolic homeostasis and overall human health and disease. Sodium butyrate (NaBu), a short chain fatty acid derived metabolite is known to modulate the inflammatory status of NASH pathogenesis; however, its mechanism of action is not clearly deciphered. To unveil the immunomodulatory activity of NaBu, we found robust anti-inflammatory effect of NaBu in diet induced NASH model with reduced macrophage infiltration. Mechanistically, independent of p65 nuclear translocation, by maintaining the enhanced acetylation status of p65 along with differential p65 recruitment to the proinflammatory gene promoter, NaBu suppressed the inflammatory milieu and resulted in better prognosis. Along with transcriptional rewiring, NaBu also altered the metabolic status, modified the functional outcome and exhibited differential secretome which ultimately resulted skewing of macrophages towards a prohealing phenotype and induced autocrine as well as paracrine death of proinflammatory macrophages to abrogate inflammation in both isolated LMs and in vivo model.
2023-01-15 | GSE219093 | GEO
Project description:This SuperSeries is composed of the SubSeries listed below.
2023-01-15 | GSE219094 | GEO
Project description:RAW264.7 murine macrophages treated with LPS
2008-06-11 | E-GEOD-1459 | biostudies-arrayexpress
Project description:Analysis of sodium butyrate（NaBu） on angiotensin II（Ang II-induced cardiac fibrosis at gene expression level. The hypothesis tested in the present study was that NaBu influence the balance of gene expression of Ang II-induce cardiac fibrosis. Results provide important information of the response of NaBu to cardiac fibrosis, such as specific genes, up- or down-regulated specific cardiac cellular functions.
2021-12-01 | GSE142436 | GEO
Project description:Label free analysis of the secretome of RAW264.7 murine macrophages in response to LPS stimulation.
2015-11-30 | PXD001905 | Pride
Project description:Alterations in Lpin2 encoding the phosphatidate phosphatase Lipin2 cause the autoinflammatory disorder Majeed syndrome. Lipin2 deficiency enhances lipopolysaccharide (LPS)-induced NLRP3 inflammasome formation in macrophages.
2021-02-16 | GSE166741 | GEO
Project description:Paeony root has long been used for its anti-inflammatory effects. In this study, the effects of albiflorin, paeoniflorin, and paeonol, compounds from paeony root, on gene expression profiles were examined in macrophages. The RAW264.7 macrophages were treated with LPS in the presence or absence of albiflorin, paeoniflorin, or paeonol. Global mRNA expression levels were detected by using an oligonucleotide microarray platform covering the mouse whole genome. Our results demonstrate that paeonol has extensive inhibitory effects on the regulation of inflammation-associated gene expression by LPS in macrophages. In addition, the predominant effect of paeonol among the tested compounds suggests that paeonol may be a major ingredient for the anti-inflammatory effect of paeony root. Keywords: RAW264.7; macrophage; inflammation; LPS; Paeony root components; dose response
2008-10-01 | GSE9632 | GEO
Project description:Purpose: Next-generation sequencing (NGS) has revolutionized systems-based analysis of cellular pathways. The goals of this study are to evaluate the gene expression of M1-polarized RAW264.7 cells compared with M0 RAW264.7 cells. Methods: RAW264.7 cells were polarized toward M1 using LPS and IFN-γ. M0 RAW264.7 cells were maintained in culture without LPS and IFN-γ. Total RNA of M1 and M0 RAW264.7 cells was extracted. RAW264.7 cells RNA profiles were generated by deep sequencing for two groups (M1 versus M0 RAW264.7 cells) with three samples each. Results: There were significant differences between M1 and M0 RAW264.7 cells. Conclusions: Polarization of RAW264.7 cells from M0 to M1 induces various changes at the transcription level.
2024-03-31 | GSE183077 | GEO
Project description:Setd1bKO primary murine bone marrow-derived macrophages (BMDMs) were treated with lipopolysaccharide (LPS) or dexamethasone and LPS (Dex+LPS) and gene expression differences in response to treatment analysed by PolyA RNA-Sequencing. No Dex-treatment dependent gene expression differences were identified. Setd1aDel/+ Raw264.7 cells with reduced Setd1a expression were analyzed with regards to their reponse to Dex when inflammatorily challenged with LPS by mRNA-Seq. We observed reduced GR-dependent gene acivation in Setd1a hypermorphic Raw264.7 cells. Wild type and Setd1aDel/+ Raw264.7 cells were treated with LPS or LPS and interferon beta (IFNB1) to show the IFNB1-dependent loss of gene expression in LPS-stimulated Setd1aDel/+ cells.
2020-12-31 | GSE137944 | GEO
Project description:Inflammation is beneficial when it is part of the innate immune response, but harmful when it occurs in an unregulated, chronic manner. We now report that IkappaB-beta, a member of the classical IkappaB family, serves a dual role of both inhibiting and facilitating the inflammatory response. IkappaB-beta degradation releases NF-kappaB dimers which upregulate proinflammatory target genes such as TNF-alpha. Suprisingly absence of IkappaB-beta results in a dramatic reduction of TNF-alpha in response to LPS even though the activation of NF-kappaB is normal. The inhibition of TNF-alpha mRNA expression can be correlated to the absence of nuclear, hypophosphorylated-IkappaB-beta bound to p65:cRel heterodimers at a specific kappaB site on the TNF-alpha promoter. Therefore IkappaB-beta acts through p65:cRel dimers to maintain prolonged expression of TNF-alpha. As a result, IkappaB-beta knockout mice are resistant to LPS induced septic shock and collagen-induced arthritis, and therefore blocking IkappaB-beta might be a promising new strategy for selectively inhibiting the chronic phase of TNF-alpha producting during the inflammatory response. Wild type and IkappaB-beta knockout BMDM cells were stimulated with LPS(1ug/ml) for 0, 1, and 5 hours. RNA isolated from the cells was analyzed on Affymetrix Mouse Genome 430A 2.0 gene expression chip.
2010-06-16 | E-GEOD-22223 | biostudies-arrayexpress