Ontology highlight
ABSTRACT:
PROVIDER: PRJNA591313 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR10520222_1.fastq.gz | Fastqsanger.gz | |||
| SRR10520222_2.fastq.gz | Fastqsanger.gz | |||
| SRR10520223_1.fastq.gz | Fastqsanger.gz | |||
| SRR10520223_2.fastq.gz | Fastqsanger.gz | |||
| SRR10520224_1.fastq.gz | Fastqsanger.gz |
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Project description:Anaerobic digestion is a popular and effective microbial process for waste treatment. The performance of anaerobic digestion processes is contingent on the balance of the microbial food web in utilizing various substrates. Recently, co-digestion, i.e., supplementing the primary substrate with an organic-rich co-substrate has been exploited to improve waste treatment efficiency. Yet the potential effects of elevated organic loading on microbial functional gene community remains elusive. In this study, functional gene array (GeoChip 5.0) was used to assess the response of microbial community to the addition of poultry waste in anaerobic digesters treating dairy manure. Consistent with 16S rRNA gene sequences data, GeoChip data showed that microbial community compositions were significantly shifted in favor of copiotrophic populations by co-digestion, as taxa with higher rRNA gene copy number such as Bacilli were enriched. The acetoclastic methanogen Methanosarcina was also enriched, while Methanosaeta was unaltered but more abundant than Methanosarcina throughout the study period. The microbial functional diversity involved in anaerobic digestion were also increased under co-digestion.
2017-01-12 | GSE93419 | GEO
Project description:Industrial anaerobic digestion (AD) represents a relevant energy source beyond today’s fossil fuels, wherein organic matter is recycled to methane gas via an intricate and complex microbial food web. Despite its potential, anaerobic reactors often undergo process instability over time, mainly caused by substrate composition perturbations, making the system unreliable for stable energy production. To ensure the reliability of AD technologies, it is crucial to identify microbial- and system responses to better understand the effect of such perturbations and ultimately detect signatures indicative of process failure . Here, we investigate the effect of microalgal organic loading rate (OLR) on the fermentation products profile, microbiome dynamics, and disruption/recovery of major microbial metabolisms. Reactors subjected to low- and high-OLR disturbances were operated and monitored for fermentation products and biogas production over time, while microbial responses were investigated via 16S rRNA gene amplicon data, shotgun metagenomics and metagenome-centric metaproteomics.
2025-02-21 | PXD048315 | Pride
Project description:The anaerobic digestion microbiomes has been puzzling us since the dawn of molecular methods for mixed microbial community analysis. Monitoring of the anaerobic digestion microbiome can either take place via a holistic evaluation of the microbial community through fingerprinting or by targeted monitoring of selected taxa. Here, we compared four different microbial community fingerprinting methods, i.e., amplicon sequencing, metaproteomics, metabolomics and phenotypics, in their ability to reflect the full-scale anaerobic digestion microbiome. The phenotypic fingerprinting reflects a, for anaerobic digestion, novel, single cell-based approach of direct microbial community fingerprinting. Three different digester types, i.e., sludge digesters, digesters treating agro-industrial waste and dry anaerobic digesters reflected different operational parameters. The α-diversity analysis yielded inconsistent results, especially for richness, across the different methods. In contrast, β-diversity analysis resulted in comparable profiles, even when translated into phyla or functions, with clear separation of the three digester types. In-depth analysis of each method's features i.e., operational taxonomic units, metaproteins, metabolites, and phenotypic traits, yielded certain similar features yet, also some clear differences between the different methods, which was related to the complexity of the anaerobic digestion process. In conclusion, phenotypic fingerprinting is a reliable, fast method for holistic monitoring of the anaerobic digestion microbiome, and the complementary identification of key features through other methods could give rise to a direct interpretation of anaerobic digestion process performance.
2021-05-26 | PXD024788 | Pride
Project description:Objective: To explore the role of GPR15L in the pathogenesis of experimental colitis and IBD. Design: We studied how genetic deletion or overexpression of Gpr15l as well as rectal application of recombinant GPR15L alter the course of acute dextran sodium sulfate (DSS) colitis. Rag1-/- and Gpr15-/- mice were used to investigate the role of T cells and Gpr15 for Gpr15l-dependent effects in acute DSS and T cell transfer colitis, respectively. The impact of GPR15L on microbiota was explored with co-housing, littermate and fecal microbiota transfer studies, by 16S rRNA sequencing as well as anti-microbial assays and anaerobic cultures of human stool suspensions analyzed by shotgun metagenomics. The expression of GPR15L was evaluated across three independent cohorts of patients with IBD and correlated to microbial diversity and flare-free survival. Results: Gpr15l clearly mitigated experimental colitis, but this was independent of T cell recruitment and Gpr15. Instead, we observed that the effects of Gpr15l were mediated by altered microbiomes in the large intestine and, consistently, showed that Gpr15l acts as an antimicrobial peptide under anaerobic conditions and shapes microbial communities towards a homeostatic phenotype. Rectal supplementation of Gpr15l counteracted experimental colitis. In patients with IBD, GPR15L expression was decreased in active inflammation, correlated with microbial diversity and was associated with flare-free survival. Conclusions: GPR15L is a host-defense peptide that plays a beneficial role in the pathogenesis of intestinal inflammation. It seems promising to further evaluate its potential as a future therapeutic approach in IBD.
2026-05-26 | GSE328435 | GEO
Project description:Objective: To explore the role of GPR15L in the pathogenesis of experimental colitis and IBD. Design: We studied how genetic deletion or overexpression of Gpr15l as well as rectal application of recombinant GPR15L alter the course of acute dextran sodium sulfate (DSS) colitis. Rag1-/- and Gpr15-/- mice were used to investigate the role of T cells and Gpr15 for Gpr15l-dependent effects in acute DSS and T cell transfer colitis, respectively. The impact of GPR15L on microbiota was explored with co-housing, littermate and fecal microbiota transfer studies, by 16S rRNA sequencing as well as anti-microbial assays and anaerobic cultures of human stool suspensions analyzed by shotgun metagenomics. The expression of GPR15L was evaluated across three independent cohorts of patients with IBD and correlated to microbial diversity and flare-free survival. Results: Gpr15l clearly mitigated experimental colitis, but this was independent of T cell recruitment and Gpr15. Instead, we observed that the effects of Gpr15l were mediated by altered microbiomes in the large intestine and, consistently, showed that Gpr15l acts as an antimicrobial peptide under anaerobic conditions and shapes microbial communities towards a homeostatic phenotype. Rectal supplementation of Gpr15l counteracted experimental colitis. In patients with IBD, GPR15L expression was decreased in active inflammation, correlated with microbial diversity and was associated with flare-free survival. Conclusions: GPR15L is a host-defense peptide that plays a beneficial role in the pathogenesis of intestinal inflammation. It seems promising to further evaluate its potential as a future therapeutic approach in IBD.
2026-05-26 | GSE327541 | GEO
Project description:Objective: To explore the role of GPR15L in the pathogenesis of experimental colitis and IBD. Design: We studied how genetic deletion or overexpression of Gpr15l as well as rectal application of recombinant GPR15L alter the course of acute dextran sodium sulfate (DSS) colitis. Rag1-/- and Gpr15-/- mice were used to investigate the role of T cells and Gpr15 for Gpr15l-dependent effects in acute DSS and T cell transfer colitis, respectively. The impact of GPR15L on microbiota was explored with co-housing, littermate and fecal microbiota transfer studies, by 16S rRNA sequencing as well as anti-microbial assays and anaerobic cultures of human stool suspensions analyzed by shotgun metagenomics. The expression of GPR15L was evaluated across three independent cohorts of patients with IBD and correlated to microbial diversity and flare-free survival. Results: Gpr15l clearly mitigated experimental colitis, but this was independent of T cell recruitment and Gpr15. Instead, we observed that the effects of Gpr15l were mediated by altered microbiomes in the large intestine and, consistently, showed that Gpr15l acts as an antimicrobial peptide under anaerobic conditions and shapes microbial communities towards a homeostatic phenotype. Rectal supplementation of Gpr15l counteracted experimental colitis. In patients with IBD, GPR15L expression was decreased in active inflammation, correlated with microbial diversity and was associated with flare-free survival. Conclusions: GPR15L is a host-defense peptide that plays a beneficial role in the pathogenesis of intestinal inflammation. It seems promising to further evaluate its potential as a future therapeutic approach in IBD.
2026-05-26 | GSE327479 | GEO
Project description:Objective: To explore the role of GPR15L in the pathogenesis of experimental colitis and IBD. Design: We studied how genetic deletion or overexpression of Gpr15l as well as rectal application of recombinant GPR15L alter the course of acute dextran sodium sulfate (DSS) colitis. Rag1-/- and Gpr15-/- mice were used to investigate the role of T cells and Gpr15 for Gpr15l-dependent effects in acute DSS and T cell transfer colitis, respectively. The impact of GPR15L on microbiota was explored with co-housing, littermate and fecal microbiota transfer studies, by 16S rRNA sequencing as well as anti-microbial assays and anaerobic cultures of human stool suspensions analyzed by shotgun metagenomics. The expression of GPR15L was evaluated across three independent cohorts of patients with IBD and correlated to microbial diversity and flare-free survival. Results: Gpr15l clearly mitigated experimental colitis, but this was independent of T cell recruitment and Gpr15. Instead, we observed that the effects of Gpr15l were mediated by altered microbiomes in the large intestine and, consistently, showed that Gpr15l acts as an antimicrobial peptide under anaerobic conditions and shapes microbial communities towards a homeostatic phenotype. Rectal supplementation of Gpr15l counteracted experimental colitis. In patients with IBD, GPR15L expression was decreased in active inflammation, correlated with microbial diversity and was associated with flare-free survival. Conclusions: GPR15L is a host-defense peptide that plays a beneficial role in the pathogenesis of intestinal inflammation. It seems promising to further evaluate its potential as a future therapeutic approach in IBD.
2026-05-26 | GSE327478 | GEO
Project description:Objective: To explore the role of GPR15L in the pathogenesis of experimental colitis and IBD. Design: We studied how genetic deletion or overexpression of Gpr15l as well as rectal application of recombinant GPR15L alter the course of acute dextran sodium sulfate (DSS) colitis. Rag1-/- and Gpr15-/- mice were used to investigate the role of T cells and Gpr15 for Gpr15l-dependent effects in acute DSS and T cell transfer colitis, respectively. The impact of GPR15L on microbiota was explored with co-housing, littermate and fecal microbiota transfer studies, by 16S rRNA sequencing as well as anti-microbial assays and anaerobic cultures of human stool suspensions analyzed by shotgun metagenomics. The expression of GPR15L was evaluated across three independent cohorts of patients with IBD and correlated to microbial diversity and flare-free survival. Results: Gpr15l clearly mitigated experimental colitis, but this was independent of T cell recruitment and Gpr15. Instead, we observed that the effects of Gpr15l were mediated by altered microbiomes in the large intestine and, consistently, showed that Gpr15l acts as an antimicrobial peptide under anaerobic conditions and shapes microbial communities towards a homeostatic phenotype. Rectal supplementation of Gpr15l counteracted experimental colitis. In patients with IBD, GPR15L expression was decreased in active inflammation, correlated with microbial diversity and was associated with flare-free survival. Conclusions: GPR15L is a host-defense peptide that plays a beneficial role in the pathogenesis of intestinal inflammation. It seems promising to further evaluate its potential as a future therapeutic approach in IBD.
2026-05-26 | GSE327477 | GEO
Project description:Objective: To explore the role of GPR15L in the pathogenesis of experimental colitis and IBD. Design: We studied how genetic deletion or overexpression of Gpr15l as well as rectal application of recombinant GPR15L alter the course of acute dextran sodium sulfate (DSS) colitis. Rag1-/- and Gpr15-/- mice were used to investigate the role of T cells and Gpr15 for Gpr15l-dependent effects in acute DSS and T cell transfer colitis, respectively. The impact of GPR15L on microbiota was explored with co-housing, littermate and fecal microbiota transfer studies, by 16S rRNA sequencing as well as anti-microbial assays and anaerobic cultures of human stool suspensions analyzed by shotgun metagenomics. The expression of GPR15L was evaluated across three independent cohorts of patients with IBD and correlated to microbial diversity and flare-free survival. Results: Gpr15l clearly mitigated experimental colitis, but this was independent of T cell recruitment and Gpr15. Instead, we observed that the effects of Gpr15l were mediated by altered microbiomes in the large intestine and, consistently, showed that Gpr15l acts as an antimicrobial peptide under anaerobic conditions and shapes microbial communities towards a homeostatic phenotype. Rectal supplementation of Gpr15l counteracted experimental colitis. In patients with IBD, GPR15L expression was decreased in active inflammation, correlated with microbial diversity and was associated with flare-free survival. Conclusions: GPR15L is a host-defense peptide that plays a beneficial role in the pathogenesis of intestinal inflammation. It seems promising to further evaluate its potential as a future therapeutic approach in IBD.
2026-05-26 | GSE327476 | GEO