Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1289364 | ENA |
REPOSITORIES: ENA
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Project description:A three-stage continuous fermentative system was developed to simulate and control physicochemical factors of the gut biology. Inoculation was of each reactor was performed from a human fecal sample which was initially amplified with a batch procedure. Samples from the initial feces, the batch and from the bioreactors media were collected to extract bacterial DNA. 16S PCR amplification was performed to assess the microbial diversity at the family level using the HuGChip. Amplified DNA was purified and labelled with either Cy3 or Cy5 dye and hybridized on the microarray.
2013-05-07 | GSE46677 | 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 | 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 | 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
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 | GSE327543 | GEO