Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Transcriptional profiling of mouse Th17 cells treated with bacterial metabolites 3-oxo-lithocholic acid [3-oxoLCA] and isolithocholic acid [isoLCA]

ABSTRACT: Transcriptional profiling of mouse Th17 cells treated with bacterial metabolites 3-oxo-lithocholic acid [3-oxoLCA] and isolithocholic acid [isoLCA]

PROVIDER: PRJNA744884 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR15070515_1.fastq.gz	Fastqsanger.gz
	SRR15070515_2.fastq.gz	Fastqsanger.gz
	SRR15070517_1.fastq.gz	Fastqsanger.gz
	SRR15070517_2.fastq.gz	Fastqsanger.gz
	SRR15070519_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 24

Similar Datasets

Transcriptional profiling of mouse Th17 cells treated with bacterial metabolites 3-oxo-lithocholic acid (3-oxoLCA) and isolithocholic acid (isoLCA)

Project description:Transcriptional profiling of mouse Th17 cells treated with bacterial metabolites 3-oxo-lithocholic acid (3-oxoLCA) and isolithocholic acid (isoLCA)

| PRJNA680248 | ENA

Transcriptional profiling of mouse Th17 cells treated with bacterial metabolites 3-oxo-lithocholic acid [3-oxoLCA] and isolithocholic acid [isoLCA]

Project description:We report transcriptional profiling of mouse Th17 cells activated and expanded in vitro in the presence of Th17-inhibitory bacterial metabolites 3-oxoLCA and isoLCA.

2021-12-10 | GSE179740 | GEO

Transcriptional profiling of mouse Th17 cells treated with bacterial metabolites 3-oxo-lithocholic acid (3-oxoLCA) and isolithocholic acid (isoLCA)

Project description:We report transcriptional profiling of mouse Th17 cells activated and expanded in vitro in the presence of Th17-inhibitory bacterial metabolites 3-oxoLCA and isoLCA.

2022-12-01 | GSE161977 | GEO

Microbial Bile acid metabolite, 3-oxo-LCA, prohibits colorectal cancer progression

Project description:Objective: Bile acids (BAs) not only influence gut microbiome composition but are also metabolized by gut bacteria to form various microbial BAs. Among these, 3-oxo-lithocholic acid (-oxo-LCA) and isoalloLCA have been reported to modulate host immunity, suppress intestinal pathogens, and provide anti-aging benefits. However, their specific effects on intestinal epithelial cells (IECs) and their role in colorectal cancer (CRC) progression remain unclear. Design: To investigate the impact of 3-oxo-LCA on intestinal tumorigenesis, we examined its effects on the growth of mouse and human CRC cell lines (CT26, MC38, HCT116), as well as on primary mouse intestinal organoids and patient-derived CRC organoids (PDCOs). Additionally, we evaluated its role in vivo using APCMin/+ mice and multiple CRC models, including syngeneic CT26 and MC38 models, as well as HCT116 and PDX-derived xenografts in NSG (immunodeficient) mice. Results: Our findings show that 3-oxo-LCA is a potent FXR agonist that restores FXR signaling both in vitro and in vivo. This results in reduced growth of CRC cell lines and suppression of intestinal stem cell (ISC)’s proliferation in both mouse organoids and PDCOs. In APCMin/+ mice, 3-oxo-LCA reduced BA levels, enhanced gut barrier function, decreased tumor burden, and blocked tumor initiation. Furthermore, it significantly inhibited tumor progression in syngeneic and xenograft mouse models and promoted apoptosis within the tumors, enhancing cancer cell death. Conclusion: These results underscore the therapeutic potential of 3-oxo-LCA as a novel FXR agonist for CRC treatment, with its ability to inhibit tumorigenesis and progression by modulating epithelial cell proliferation and inducing apoptosis.

2025-08-14 | GSE294276 | GEO

Gut-derived metabolites drive Th17 cell pathogenicity in Multiple Sclerosis

Project description:The gut-brain axis is an emerging factor in promoting multiple sclerosis (MS). However, the underlying mechanisms and strategies to target this axis are not established. Here, we investigated how the gut environment influences myelin-specific Th17 cell pathogenicity. We used the adoptive Th17 cell transfer experimental autoimmune encephalomyelitis (EAE) model and antibiotic treatment to modulate the intestinal microbiome. We observed a reduced pathogenic Th17 cell signature in the colon of antibiotics-treated mice. Treatment with fecal filtrates enhanced myelin-specific Th17 cell encephalitogenic properties both in vitro and in vivo. Feces metabolomic profiling identified altered tryptophan-derived metabolites, including indole-3-carboxylate (I3CA). Oral I3CA supplementation accelerated EAE development and I3CA concentration in blood samples from persons with MS (PwMS) was associated with increased disease severity mirrored by increased serum neurofilament light chain levels. Altogether, our study shows that microbiota-derived metabolites play a key role in the intestine during neuroinflammation, offering potential therapeutic insights for PwMS.

2025-07-15 | GSE282316 | GEO

Microbial Bile Acid Metabolites regulate Central Nervous System autoimmunity

Project description:the commensal gut microbiota modulates multiple sclerosis with unknown mechanisms. Commensal bacteria producing bile acid-deconjugating enzymes are fundamental to generate secondary bile acid metabolites (BAM) with immunoregulatory function. We show that immune regulatory BAM prevent autoimmunity in the central nervous system by inducing immune tolerance at the intestinal level and peripherally limiting effector function and aggressiveness of myelin-reactive T cells. We validated the key role of microbiota-induced BAM in humans by showing that relapsing-remitting multiple sclerosis patients have significantly reduced level of an important immune regulatory BAM (deoxycholic acid) and lower abundance of BAM-producing bacteria that correlate with increased percentages of peripheral effector Th17 cells. Our data indicate that the immune regulatory biliary network is crucial for the prevention of central nervous system autoimmunity.

2025-03-17 | GSE233771 | GEO

The maize death acids, 10-oxo-11-phytoenoic acid and derivatives, are rapidly induced phytoalexins with multiple biological activities

Project description:Plant cellular damage promotes the interaction of lipoxygenases (LOX) with free fatty acids to yield 9- and 13-hydroperoxides which are further metabolized into diverse oxylipins. The enzymatic action of 13-LOX on linolenic acid enables production of 12-oxo-phytodienoic acid (12-OPDA) and its downstream products, jointly known as jasmonates. As signals, jasmonates have related yet distinct roles in the regulation of plant resistance against insect and pathogen attack. An additional and conceptually parallel pathway involving 9-LOX activity on linoleic acid leads to the production of 10-oxo-11-phytoenoic acid (10-OPEA). Despite structural similarity to jasmonates, physiological roles for 10-OPEA have remained unclear. Both 12-OPDA and 10-OPEA equally promote the transcription of numerous defense genes encoding glutathione S-transferases, cytochrome P450s, and pathogenesis-related proteins; however, 10-OPEA activity diverges in the context of reduced protease inhibitor transcript accumulation. To identify additional differential responses, we subsequently performed whole transcriptome analyses using RNAseq. These comparisons provide a platform for further examination of plant response specificity to the cyclopentenone 10-OPEA.

2015-08-13 | GSE68589 | GEO

Saccharomyces cerevisiae TPP 2-oxo acid decarboxylases

Project description:The irreversible decarboxylation step, which commits 2-oxo acids to the Ehrlich pathway, was initially attributed to pyruvate decarboxylase. However, the yeast genome was shown to harbour no fewer than 5 genes that show sequence similarity with thiamine-diphosphate dependent decarboxylase genes. Three of these (PDC1, PDC5 and PDC6) encode pyruvate decarboxylases { while ARO10 and THI3 represent alternative candidates for Ehrlich-pathway decarboxylases. Transcriptome analysis and decarboxylase activity measurements on an S. cerevisiae aro10 strain, a double aro10 thi3 deletion strain and a quadruple pdc1,5,6,aro10 mutant strains grown in carbonâ€“limited chemostat with phenylalanine as nitrogen source indicated that: i) PDC5 is strongly upregulated in an aro10 background (Fig. 2) and also encodes a broad-substrate Î±-keto acid decarboxylase. ii) PDC5 expression depends on the presence of THI3 (Fig. 2), and iii) in contrast to cell extracts from a strain expressing ARO10 only (pdc1,5,6, thi3), cell extract from a strain that only contains THI3 (pdc1,5,6,aro10) did not produce any Î±-keto acid decarboxylase activity . THI3 has recently been demonstrated to be involved in regulation of thiamine homeostasis in S. cerevisiae, which further suggests that its role in the Ehrlich pathway may be regulatory rather than catalytic. A systematic investigation of the catalytic properties of all five (putative) TPP-dependent decarboxylases (Aro10p, Thi3p, Pdc1p, Pdc5p, Pdc6p) is essential for a final resolution of the substrate specificity of these key enzymes in the Ehrlich pathway. Keywords: Strain comparison

2007-11-15 | GSE9590 | GEO

Microbial Bile acid metabolite, 3-oxo-LCA, prohibits colorectal cancer progression

Project description:Microbial Bile acid metabolite, 3-oxo-LCA, prohibits colorectal cancer progression

| PRJNA1248922 | ENA

Gut-derived metabolites drive Th17 cell pathogenicity in Multiple Sclerosis

Project description:Gut-derived metabolites drive Th17 cell pathogenicity in Multiple Sclerosis

| PRJNA1188120 | ENA