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Alistipes putredinis protects DSS-induced colitis through mediating immune tolerance

ABSTRACT: Alistipes putredinis protects DSS-induced colitis through mediating immune tolerance

PROVIDER: PRJNA1037524 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26772151_1.fastq.gz	Fastqsanger.gz
	SRR26772151_2.fastq.gz	Fastqsanger.gz
	SRR26772152_1.fastq.gz	Fastqsanger.gz
	SRR26772152_2.fastq.gz	Fastqsanger.gz
	SRR26772153_1.fastq.gz	Fastqsanger.gz

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Alistipes putredinis protects DSS-induced colitis through mediating immune tolerance

Project description:Alistipes putredinis can alleviate DSS-induced colitis in mice, but the mechanism is unknown. The aim of this study was to examine the changes in gene expression in the intestinal tissue of mice with colitis following treatment with Alistipes putredinis by RNA sequencing.

2024-12-31 | GSE247421 | GEO

Alistipes putredinis CAG:67

Project description:Alistipes putredinis CAG:67 overview

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Enterobacter ludwigii protects DSS-induced colitis through choline-mediated immune tolerance

Project description:Commensal intestinal bacteria play key roles in regulating cells mediating immune tolerance; however, bacterial strains and related metabolites directly involved in this regulation are largely unknown. Here, using a mouse model of dextran sulfate sodium (DSS)-induced colitis combined with different antibiotic treatment, Enterobacter ludwigii, abundant in microbiota of mice treated with metronidazole, was screened out to have prophylactic and therapeutic effects on DSS-induced colitis with or without the presence of complex intestinal bacteria. E. ludwigii was demonstrated to induce CD103+DC and Treg-mediated immune tolerance for colitis remission using in vitro and in vivo experiments. Moreover, choline, one of E. ludwigii metabolites, was identified to increase DCs’ immune tolerance to promote Treg differentiation. E. ludwigii was found to induce DCs’ immune tolerance ability for Treg differentiation through choline and α7nAChR-mediated RA and TGF-β upregulation, resulting in protecting mice against DSS-induced colitis. This study provides potential therapeutic approaches for IBD.

2024-08-05 | MTBLS5585 | MetaboLights

Paneth cell SIRT1 deficiency protects against DSS-induced colitis

Project description:Paneth cells, intestine-originated innate immune-like cells, are important for maintenance of the intestinal stem cell niche, gut microbiota, and gastrointestinal barrier. Dysfunctional Paneth cells under pathological conditions are a site of origin for intestinal inflammation. However, mechanisms underlying stress-induced Paneth cell dysregulation remains unclear. We have previously reported that deletion of SIRT1 in the intestinal epithelium (SIRT1 iKO) leads to hyperaction of Paneth cells along with an increased sensitivity to Dextran sodium sulfate (DSS)-induced colitis. We recently generated a Paneth-cell specific SIRT1 KO mouse model (SIRT1 PKO). Similar to mice with SIRT1 iKO mice, SIRT1 PKO mice had increased abundance as well as hyperactivation of Paneth cells in vivo and in cultured intestinal organoids. However, in contrast to the hypersensitivity of SIRT1 iKO mice to chemical- or age-induced inflammation, SIRT1 PKO mice were protected from Dextran sodium sulfate (DSS)-colitis.

2025-03-31 | GSE262546 | GEO

Alistipes putredinis

Project description:Normal gastrointestinal bacterium

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TFEB target in epithelial cells during DSS colitis

Project description:TFEB in IEC has a protective role in DSS colitis. The goal is to examine what genes/pathways are TFEB target during DSS colitis

2018-02-22 | GSE98266 | GEO

Polydatin protects against DSS-induced ulcerative colitis via Nrf2/Slc7a11/Gpx4-dependent inhibition of ferroptosis signalling activation

Project description:Ulcerative colitis (UC), a form of inﬂammatory bowel disease, is characterized by a Q7 recurrent and persistent nonspeciﬁc inﬂammatory response. Polydatin (PD), a natural stilbenoid polyphenol with potent properties, exhibits unexpected beneﬁcial effects beyond its well-documented anti-inﬂammatory and antioxidant activities. In this study, we presented evidence that PD confers protection against dextran sodium sulfate (DSS)-induced ulcerative colitis. Our ﬁndings demonstrated that PD mitigated the DSS-induced increases in proinﬂammatory cytokines (IL-6, TNF-α, and IL-1β), alleviated colon length shortening, reduced morphological damage to the intestinal mucosa, and preserved tight junction proteins (TJ) occludin and Zonula occludens-1 (ZO-1) in both Caco-2 cells and murine models of colitis. Results from bulk RNA sequencing and differential gene analysis suggested a potential role for ferroptosis in the protective mechanisms of PD against UC. Further investigations revealed that PD modulated the expression levels of several ferroptosis-related proteins and transcription factors within the DSS-induced colitis model. Notably, treatment with PD enhanced nuclear translocation of Nrf2, which inhibits ferroptosis while ameliorating oxidative stress through upregulation of Slc7a11 and Gpx4 expression. Additionally, erastin—a known inducer of ferroptosis—reversed the protective effects conferred by PD in the DSS-induced colitis model by downregulating Slc7a11 expression. These ﬁndings underscore that PD protects against DSS-induced ulcerative colitis via the Nrf2/ Slc7a11/Gpx4 signaling axis, highlighting its potential as a novel therapeutic agent for UC.

2025-01-07 | GSE285956 | GEO

Effect of DSS Colitis on Meninges

Project description:The Meninges of mice which were treated with DSS to induce colitus were compared to control mice.

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Gene expression profiles of mouse colitis epithelial tissues induced by DSS or DSS/PhIP

Project description:We reported the gene expression profiles of hCYP1A mouse colitis epithelial tissues on Day 1, 3 and 7 after the treatment with DSS or DSS/PhIP for 5 days.

2019-09-14 | GSE137387 | GEO