Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Metabolomics in mice serum T_Suzuki Protocol 2

ABSTRACT: Quantification of indolelactic acid (ILA), indoxyl sulfate, indole-3-propionic acid, cortisol, tryptophan, thyroxine (T4), kynurenine and serotonin

INSTRUMENT(S): impact II

ORGANISM(S): Mus Sp. (ncbitaxon:10095)

SUBMITTER: Ruth Ley

PROVIDER: MSV000097925 | MassIVE | Tue May 20 03:22:00 BST 2025

REPOSITORIES: MassIVE

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Gut-derived indole propionic acid alleviates liver fibrosis by modulating pro-fibrogenic macrophage phenotype and biological function

Project description:Recently, gut metabolites have been recognized to play significant roles in liver diseases via the gut-liver axis. In this study, we investigate the regulatory effects of the tryptophan metabolite, indole-3-propionic acid (IPA), on immune cells during liver fibrogenesis using single-cell RNA sequencing (scRNA-seq).

2024-09-20 | GSE277148 | GEO

Metabolomics in mice serum T_Suzuki Protocol 1

Project description:Quantification of corticosterone, glutamic acid, 9 kynurenic acid and GABA.

2025-05-20 | MSV000097923 | MassIVE

GNPS - Metabolomics in mice serum T_Suzuki Protocol 1

Project description:Quantification of corticosterone, glutamic acid, 9 kynurenic acid and GABA.

2025-05-20 | MSV000097923 | GNPS

RNA sequencing of L4-L6 mouse Dorsal Root Ganglia 3 days post sciatic nerve crush and naive following 10 days of Indole-3-propionic acid treatment

Project description:Purpose: compare the response of DRG neurons to indole-3-propionic acid treatment before and after sciatic nerve injury Results: we found that IPA induced transcription changes before and after injury inside the DRG tissue. In particular expression of immune system related genes

2022-01-01 | GSE161342 | GEO

A Sinorhizobium meliloti IAA-overproducing strain improves phosphate solubilization and Medicago plant yield

Project description:This SuperSeries is composed of the following subset Series: GSE21735: Sinorhizobium meliloti cells: untreated 1021 strain vs. 1021 treated with 2,4-dichlorophenoxyacetic acid (2,4-D) GSE21737: Sinorhizobium meliloti cells: untreated 1021 strain vs. 1021 treated with indole-3-acetic acid (IAA) GSE21740: Sinorhizobium meliloti cells: untreated 1021 strain vs. 1021 treated with indole-3-carboxylic acid (ICA) GSE21742: Sinorhizobium meliloti cells: untreated 1021 strain vs. 1021 treated with indole (IND) GSE21743: Sinorhizobium meliloti cells: untreated 1021 strain vs. 1021 treated with tryptophan (Trp) GSE21744: Sinorhizobium meliloti cells: untreated 1021 wild type strain vs. RD64 strain Refer to individual Series

2010-05-20 | E-GEOD-21745 | biostudies-arrayexpress

Project description:Clostridium sporogenes and its tryptophan metabolite indole-3-propionic acid repair antibiotic-induced muscle atrophy in mice

| PRJNA1283927 | ENA

Lactobacillus intestinalis

Project description:Lactobacillus intestinalis-derived indole-3-propionic acid mediates benefits of maternal tryptophan metabolism on offspring intestinal health

| PRJNA721108 | ENA

Microbiota-dependent indole production is required for the development of collagen-induced arthritis

Project description:Altered tryptophan catabolism has been identified in inflammatory diseases like rheumatoid arthritis (RA) and spondyloarthritis (SpA), but the causal mechanisms linking tryptophan metabolites to disease are unknown. Using the collagen-induced arthritis (CIA) model we identify alterations in tryptophan metabolism, and specifically indole, that correlate with disease. We demonstrate that both bacteria and dietary tryptophan are required for disease, and indole supplementation is sufficient to induce disease in their absence. When mice with CIA on a low-tryptophan diet were supplemented with indole, we observed significant increases in serum IL-6, TNF, and IL-1β; splenic RORγt+CD4+ T cells and ex vivo collagen-stimulated IL-17 production; and a pattern of anti-collagen antibody isotype switching and glycosylation that corresponded with increased complement fixation. IL-23 neutralization reduced disease severity in indole-induced CIA. Finally, exposure of human colon lymphocytes to indole increased expression of genes involved in IL-17 signaling and plasma cell activation. Altogether, we propose a mechanism by which intestinal dysbiosis during inflammatory arthritis results in altered tryptophan catabolism, leading to indole stimulation of arthritis development. Blockade of indole generation may present a novel therapeutic pathway for RA and SpA.

2023-11-13 | GSE241655 | GEO

Proteomic characterization of the cellular effects of AHR activation by microbial tryptophan catabolites in endotoxin-activated human macrophages

Project description:Sensing of microbial tryptophan catabolites by the aryl hydrocarbon receptor (AhR) plays a pivotal role in host-microbiome homeostasis by modulating the host immune response. Thereby the involved cellular processes triggered by the metabolites are largely unknown. We analyzed proteomic changes in macrophages trough 24h after treatment with the tryptophan metabolites indole-3-acetic acid (I3AA) or indole-3-aldehyde (IAld), as well as the prototypic AhR-ligand Benzo(a)pyrene (BaP) in the absence and presence of LPS to identify affected processes and pathways.

2021-11-03 | PXD025022 | Pride

Atorvastatin improved ulcerative colitis in association with gut microbiota-derived tryptophan metabolism

Project description:Aims: Atorvastatin is a commonly used cholesterol-lowering drug that possesses non-canonical anti-inflammatory properties. However, the precise mechanism underlying its anti-inflammatory effects remains unclear. Materials and methods: The acute phase of ulcerative colitis (UC) was induced using a 5 % dextran sulfate sodium (DSS) solution for 7 consecutive days and administrated with atorvastatin (10 mg/kg) from day 3 to day 7. mRNA-seq, histological pathology, and inflammatory response were determined. Intestinal microbiota alteration, tryptophan, and its metabolites were analyzed through 16S rRNA sequencing and untargeted metabolomics. Key findings: Atorvastatin relieved the DSS-induced UC in mice, as evidenced by colon length, body weight, disease activity index score and pathological staining. Atorvastatin treatment reduced the level of pro_x0002_inflammatory cytokines interleukin-6 (IL-6) and tumor necrosis factor alpha (TNF-α). Atorvastatin also relieved the intestinal microbiota disorder caused by UC and decreased the proliferation of pernicious microbiota such as Akkermansia and Bacteroides. Atorvastatin dramatically altered tryptophan metabolism and increased the fecal contents of tryptophan, indolelactic acid (ILA), and indole-3-acetic acid (IAA). Furthermore, atorvastatin enhanced the expression level of aryl hydrocarbon receptor (AhR) and interleukin-22 (IL-22) and further promoted the expression level of intestinal tight junction proteins, such as ZO-1 and occludin, in colitis mice. Significance: These findings indicated that atorvastatin could alleviate UC by regulating intestinal flora disorders, promoting microbial tryptophan metabolism, and repairing the intestinal barrier.

2024-11-04 | GSE280960 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data