Ontology highlight
ABSTRACT:
PROVIDER: PRJNA874684 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR21292646_1.fastq.gz | Fastqsanger.gz | |||
| SRR21292646_2.fastq.gz | Fastqsanger.gz | |||
| SRR21292647_1.fastq.gz | Fastqsanger.gz | |||
| SRR21292647_2.fastq.gz | Fastqsanger.gz | |||
| SRR21292648_1.fastq.gz | Fastqsanger.gz |
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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: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.
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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.
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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.
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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.
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