Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1147270 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:By performing RNA-seq analysis on ALKBH5-deficient (ALKBH5-/-, KO) and Wild-type (WT) dHL-60 human neutrophils infected with Escherichia coli, we want to investigate the effect of ALKBH5 on transcriptional landscape of human neutrophils during bacterial infection. Then, we performed gene expression profiling and Gene Ontology enrichment analysis of the significantly differentially expressed genes using data obtained from RNA-seq.
2023-12-21 | GSE224650 | GEO
Project description:By performing m6A-seq analysis on dHL-60 human neutrophils infected with Escherichia coli, we want to identify the m6A methylation pattern in neutrophils after bacteria challenge. m6A-seq analysis revealed that the consensus m6A motifs were most significantly enriched within the m6A peaks with typical m6A peak distribution features, and m6A methylation sites were located primarily in the protein coding sequence region and 3′ untranslated region of mRNA transcripts, in neutrophils with bacterial infection.
2022-05-24 | GSE201060 | GEO
Project description:The purpose of the present study was to elucidate the exocytic events in neutrophil-mediated inflammation. Therefore, we first investigated the expression of genes implicated in these exocytic events in a cell model for neutrophils, the promyelocytic HL-60 cell line. By the addition of 1.3% DMSO during 4.5 days, these cells are differentiated into neutrophil-like dHL-60 cells. Non-differentiated cells served as control. Upon cell differentiation, we i) identified differentially expressed genes implicated in the mechanisms of vesicle transport, and ii) found some of them being upregulated. This upregulated gene expression upon DMSO-maturation points towards a functional role in these cells. Secondly, we confirmed the expression of the selected genes in human neutrophils, isolated from venous blood of 4 different donors.
2014-11-25 | E-MTAB-2107 | biostudies-arrayexpress
Project description:To uncoverthe capsaicin effects on the neutrophil activation, we performed transcriptomic of dHL-60 cells after capsaicin stimulation in degree of different time. this study revealed the functional changes of neutrophils in the presence of capsaicin. The transcriptomic data with different time stimulation gradients can contribute to the revealing of dynamic alternation in gene expression and annotate the time-dependent effect of the neutrophil respond to capsaicin.
2022-06-30 | GSE198304 | GEO
Project description:Transcriptome-wide m6A Methylation Profiling of dHL-60 human neutrophils by m6A-seq
| PRJNA828163 | ENA
Project description:Neutrophils play a central role in the inflammatory and reparative processes following myocardial infarction (MI), and can switch between pro-inflammatory (N1) and reparatory (N2) states, influencing disease outcomes. Mesenchymal stromal cells (MSC), known for their immunomodulatory effects, may hold the key to controlling neutrophil behaviour. In this study, we explored how MSC influence neutrophil states both in vitro and in vivo in an MI mouse model. We developed a reliable system to study neutrophils by differentiating HL-60 cells into neutrophil-like cells (dHL-60). These cells were polarized into N1 and N2 types, showing distinct protein markers and cytokine signatures. When exposed to MSC, pro-inflammatory N1 cells reduced their production of inflammatory signals (TNFα, MCP-1), while N2 cells increased their reparatory signals (IL-10, TGM2). In mice with MI, MSC reduced the number of neutrophils migrating to damaged heart tissue and altered their transcriptomic signatures. Surprisingly, MSC enhanced inflammatory pathways in heart neutrophils while dampening their ability to support tissue repair. These findings underscore the complex role of MSC in modulating neutrophil responses, demonstrating a nuanced impact on inflammatory and reparative pathways in the cardiac microenvironment. While the results highlight MSC' potential to influence immune cell behaviour, they also reveal context-specific effects that warrant further investigation to fully elucidate their therapeutic implications in cardiovascular disease.
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Project description:Severe combined immunodeficiency 8 (IMD8) is caused by mutations in the human Coronin 1A (Coro1A). The clinical presentation of IMD8 patients is characterized by recurrent bacterial infections, suggesting an important role of Coro1A in innate immunity. To analyze the molecular mechanism of Coro1A during neutrophil recruitment, we identified the Coro1A interactome by conducting co-immunoprecipitation (Co-IP) experiments using GFP NanoTrap technology and subsequent mass spectrometry (LC-MS/MS) using human neutrophil-like differentiated HL-60 (dHL-60) cells stably expressing Coro1A-EGFP (dHL-60-Coro1A-EGFP) cells.
2017-06-29 | PXD004635 | Pride
Project description:The purpose of the present study was to elucidate in more details the molecular mechanisms of neutrophil-mediated inflammation. We therefore investigated the time-dependent stimulatory potential of LPS from Escherichia coli on cytokine response in neutrophil-like HL-60 cells. <br><br>To get a general overview on the total mRNA changes in DMSO-differentiated HL-60 cells, we performed whole-transcript analysis of LPS-stimulated dHL-60 cells after 2h and 6h of LPS treatment. The samples were collected from three independent experiments from three different passages in cell culture. Non-stimulated dHL-60 cells served as control. We identified the differentially expressed cytokine genes implicated in the human inflammatory response and prominent for their role in neutrophil-mediated inflammatory processes.
2014-12-17 | E-MTAB-1393 | biostudies-arrayexpress