Microbial communities in plastic fishing nets
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB62111 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:To investigate the altered gene expression levels in BMDMs treated with or without NETs. Each group had a biological repeat (n=3). Results provide insight into the effect of NETs on BMDMs.
2024-11-27 | GSE268729 | GEO
Project description:Although the formation of neutrophil extracellular traps (NETs) is caused by inflammation-related factors, it remains unclear whether endogenous hormones promote NET formation. Here, we investigate NET formation between infection-driven inflammatory endometrium and estrogen-induced hyperplastic endometrium by single-cell multiomics analysis. We identified a unique neutrophil subpopulation (CD24high neutrophil) involved in estrogen-driven NET formation. Estrogen-induced NETs mainly form due to the imbalance of histone caused by estrogen receptors. Inhibition of NETs significantly ameliorated endometrial hyperplasia (EH) in a murine model. Mechanistically, NETs promote cell proliferation by binding to NKCC1 on epithelial cells. Aspirin was screened to inhibit NET formation and alleviated EH in cynomolgus monkey. This study provides a novel nonhormone replacement therapy to treat patients with estrogen abnormalities by targeting NETs.
2025-01-29 | GSE223639 | GEO
Project description:Background Adenosine Deaminase 2 Deficiency (DADA2) is an autoinflammatory disease characterized by systemic vasculopathy, strokes and mild immunodeficiency. Recently NETosis has been implicated in the pathogenesis of Deficiency of Adenosine Deaminase 2. Objectives To deep investigate the possible effects of NETs on the immune system we characterized proteomic profile of NETs from DADA2 as compared to HD and Polyarteritis Nodosa (PAN) patients. To determine if NETs contain possibly immunogenic antigens we study functional aspects on Dendritic Cells after in vitro stimulation with NETs. Methods Twenty two DADA2 patients were enrolled. We analyzed NETosis by Imaging Flow Citometry. We evaluated NETs remnants and DNAse in the plasma samples by ELISA assay whereas DNAse activity by DNA digestion. We used quantitative proteomics approach to identify NET proteins in 6 DADA2, 7 PAN and 7 HD. Results Neutrophils from DADA2 patients show a significant increased suicidal NETosis. DNAse enzymes were not normal in the level or activity. By proteomic analysis we identified 1356 proteins among which a hundred of proteins were significantly up or down-modulated in DADA2 NETs as compared to controls NETs in resting condition and after stimulation with PMA, Adenosine and TNFα. DADA2 NETs are significantly more efficient than normal NETs in stimulating patients’ monocyte-derived dendritic cells. Conclusion We identified different pathways significantly upregulated or downregulated in DADA2 NETs versus PAN/HD NETs. This peculiar protein profile could be contribute to activate inflammatory pathways in Dendritic cells in DADA2.
2025-06-23 | PXD055246 | Pride
Project description:We reported the application of RNA sequecing to broadly understand the pathways associated with HUVECs exposed to vehicle, NETs, or NETs + defibrotide. We identified 440 differentially expressed genes (300 upregulated) in HUVECs upon NET stimulation as compared with vehicle. Conversely, there were 229 differentially expressed genes (192 downregulated) when the NETs + defibrotide group was compared to NETs alone.
2021-10-13 | GSE179828 | GEO
Project description:The study aimed to explore the potential of bacterial biodegradation as a solution to the global problem of plastic pollution, specifically targeting polyethylene (PE), one of the most common types of plastic. The goals of the study were to isolate a bacterial strain capable of breaking down PE, identify the key enzymes responsible for the degradation process, and understand the metabolic pathways involved. By investigating these aspects, researchers sought to gain critical insights that could be used to optimize plastic degradation conditions and inform the development of artificial microbial communities for effective bioremediation strategies. This research has significant relevance, as it addresses the pressing need for innovative and sustainable approaches to tackle the ever-growing issue of plastic waste and its impact on the environment.
2024-01-02 | PXD041981 | Pride
Project description:Gastroenteropancreatic neuroendocrine tumors (GEP-NETs) are rare and heterogeneous tumors presenting a wide spectrum of different clinical and biological characteristics. In these tumors, the histological evaluation is a crucial element of clinical management. Currently, tumor grading, determined by Ki-67 staining and mitotic counts, is the most reliable predictor of prognosis. This scoring method is time-consuming and a high reproducibility cannot be achieved. Novel approaches are needed to support histological evaluation and prognosis. In this study, starting from a microarray analysis, we defined the miRNAs signature for poorly differentiated NETs (G3) compared to well differentiated NETs (G1 and G2) consisting of 56 deregulated miRNAs. Moreover, we identified 8 miRNAs that were expressed in all GEP-NETs grades but at different level. Among these miRNAs, we found miR-96-5p that raised its expression levels from grade 1 to grade 3; inversely, its target FOXO1 was decrease from grade 1 to grade 3. Our results reveal that the miRNAs expression profile of GEP-NET correlates their expression with grading showing a potential advantage of miRNA quantification to aid clinicians in the classification of common GEP-NETs subtypes.
2020-08-04 | GSE135034 | GEO
Project description:Chemotherapy-induced peripheral neuropathy (CIPN) is a serious adverse reaction of chemotherapy with limited treatment. Previous research indicates neutrophil extracellular traps (NETs) is a critical pathogenesis of CIPN. LPS/HMGB1 serve as important inducers of NETs. Here, we aim to target inhibiting NETs formation (NETosis) to alleviate CIPN. Clinically we found the content of LPS, HMGB1 and NETs in the plasma of CIPN patients was significantly increased and positively correlated with VAS scores. Fucoidan decreased LPS/HMGB1/NETs content and relieved CIPN in mice. Mechanistically, fucoidan upregulated the scavenger receptor A1 (SR-A1) expression and promoted bone marrow derived macrophage (BMDM) to phagocytize LPS/HMGB1. Fucoidan also facilitated BMDM to engulf NETs via the recognition and localization of SR-A1 and HMGB1. The therapeutic effects of fucoidan were abolished by SR-A1 knockout. RNA-seq analysis showed that fucoidan significantly increased sqstm1 (p62) gene expression. Fucoidan promoted the competitive binding of sqstm1 and Nrf2 to Keap1, increasing Nrf2 nuclear translocation and SR-A1 transcription. Additionally, microbial diversity sequencing analysis (16S) showed that fucoidan increased gut microbiota diversity and abundance, and upregulated the Bacteroides/Firmicutes ratio. In conclusion, fucoidan promotes SR-A1-mediated phagocytosis of LPS/HMGB1/NETs and maintains gut microbial homeostasis, providing a potential therapeutic strategy for CIPN.
2025-04-09 | GSE249275 | GEO
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
Project description:Neutrophil extracellular traps (NETs) promote inflammation and atherosclerosis progression. In diabetes they are increased and impair wound healing, during which inflammation normally resolves. Atherosclerosis regression, a process resembling wound healing, is also impaired in diabetes. Thus, we hypothesized that NETs impede atherosclerosis regression in diabetes through unresolved inflammation. Objective: To investigate in diabetes the effect of NETs on plaque macrophage inflammation and whether NETs reduction improves atherosclerosis regression. Findings: Transcriptomic profiling of plaque macrophages from NET positive and negative areas in Ldlr-/- mice revealed inflammasome and glycolysis pathway upregulation, indicating a pro-inflammatory phenotype. During atherosclerosis regression in non-diabetic mice, plaque NET content decreased. In contrast, in diabetic mouse plaques NETs were enriched and persisted after lipid-lowering. DNase1 treatment (to degrade NETs) of diabetic mice reduced plaque NETs and macrophage inflammation and improved atherosclerosis regression after lipid-lowering. Conclusions: NETs decline during atherosclerosis regression in non-diabetic mice, but persist in diabetes and impair regression by exacerbating macrophage inflammation. DNase1 reduced diabetic plaque NETs and macrophage inflammation, and restored atherosclerosis resolution after lipid-lowering, despite ongoing hyperglycemia. Given that humans with diabetes also exhibit impaired atherosclerosis resolution with lipid-lowering, these data suggest that NETs contribute to the increased CVD risk in this population.
2020-05-12 | GSE145200 | GEO