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Homo sapiens

ABSTRACT: Raw sequence reads of Homo sapiens Neutrophil Extracellular Traps (NETs)

PROVIDER: PRJNA587717 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10398045_1.fastq.gz	Fastqsanger.gz
	SRR10398045_2.fastq.gz	Fastqsanger.gz
	SRR10398046_1.fastq.gz	Fastqsanger.gz
	SRR10398046_2.fastq.gz	Fastqsanger.gz
	SRR10398047_1.fastq.gz	Fastqsanger.gz

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Transcriptome sequencing analysis of naïve CD4+ T cells treated with NETs or control vehicle

Project description:Purpose: We found neutrophil extracellular traps (NETs) can affect the differentiation of naïve CD4+ T cells. This sequencing aims to explore the gene profile change of neutrophil extracellular traps (NETs) on naïve CD4+ T cells. Methods: Total RNA was extracted from the T cells treated with NETs or vehicle for 72h and send to sequencing. Sequencing libraries were generated using NEBNext®UltraTMRNA Library Prep Kit for Illumina® (NEB, USA) and sequenced on an Illumina platform. Paired-end reads were then generated and evaluated for quality control. Clean raw data with high quality were aligned to the reference genome using the Spliced Transcripts Alignment to a Reference (STAR) software. For quantification, FeatureCouts was used to count the read numbers mapped of each gene. Differential expression analysis between two groups (three biological replicates per condition) was performed using DESeq2 R package. Results: Using an optimized data analysis workflow, we mapped around 40 million sequence reads per sample with total mapping rate around 96%. Total 23,249 transcripts in the NETs and Vehicle group were identified. Approximately 7% of the transcripts (1675) showed differential expression between the with p value <0.05. Top differential expressed genes were then enriched based on KEGG and GO database. Altered expression genes in the most enrichment pathways were confirmed with qRT–PCR and western blot, demonstrating the high degree of sensitivity of the RNA-seq method. The top differential expressed genes provide new insigts for the mechanism of T cell differentiation affected by NETs. Conclusions: Our study represents the first detailed analysis of naïve CD4+ T cells treated with NETs. Most differentital expressed genes were enriched in metabolic pahtways, which prompted us to further explore the related mechanism of the novel phenotype.

2021-12-10 | GSE161464 | GEO

Neutrophil extracellular traps mediate articular cartilage damage and enhance the immunogenicity of cartilage components in rheumatoid arthritis

Project description:This study invesigates the effects of neutrophil extracellular traps (NETs) on articular cartilage degredation and resulting autoimmune responses in rheumatoid arthritis.

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Project description:Cell Cycle Proteins Control Production of Neutrophil Extracellular Traps (NETs)

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Homo sapiens whole blood.

Project description:RNA extracted at 240min. Samples are rRNA depleted. Expression measurement of Homo sapiens genes.

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Neutrophil extracellular trap induced dendritic cell activation leads to Th1 polarization in type 1 diabetes

Project description:We performed a comparison of transcriptome between monocyte-derived dendritic cells (moDC) cultured with neutrophil extracellular traps (NETs) from healthy donors or type 1 diabetes (T1D) patients. The source of moDCs is healthy donors and T1D patients

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Homo sapiens whole blood infected with Candida spp. (here: Candida parapsilosis)

Project description:Homo sapiens fresh whole blood was infected with Candida parapsilosis. RNA-pool of both species extracted at 0min (control), 15, 30, 60, 120, 240 min. Samples are rRNA depleted. Measurement of Homo sapiens gene expression.

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Project description:Neutrophil recruitment and activation are hallmarks of the prevalent inflammatory disease, periodontitis. However, the mechanisms by which neutrophils contribute to in inflammatory bone destruction remain unclear. Herein, we document that neutrophil extracellular traps (NETs) have a direct role in mediating inflammatory pathology. In an established animal model of periodontitis, we demonstrate that genetic or pharmacologic inhibition of NETs formation, or removal of NETs by DNase-Ⅰ, alleviates inflammatory bone loss in vivo. Investigating the mechanisms by which NETs drive periodontal inflammation, we find that extracellular histones have a direct role in disease progression. Consistent with findings in animal models, histones bearing classic NET-associated post-translational modifications are correlated with disease severity and are significantly elevated in local lesions and systemic circulation of patients with periodontitis. Our work reveals NETs-associated components as pathogenic mediators, potential biomarkers, and therapeutic targets for periodontitis.

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