Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Lactobacilli modulate epithelial cytoprotection through the Nrf2 pathway

ABSTRACT: Lactobacilli modulate epithelial cytoprotection through the Nrf2 pathway

PROVIDER: PRJNA294320 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR2221901_1.fastq.gz	Fastqsanger.gz
	SRR2221901_2.fastq.gz	Fastqsanger.gz
	SRR2221902_1.fastq.gz	Fastqsanger.gz
	SRR2221902_2.fastq.gz	Fastqsanger.gz
	SRR2221903_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 8

Similar Datasets

Lactobacilli modulate epithelial cytoprotection through the Nrf2 pathway [RNA-Seq]

Project description:We report that cellular ROS enzymatically generated in response to contact with lactobacilli in both mice and Drosophila has salutary effects against exogenous insults to the intestinal epithelium via the activation of Nrf2 responsive cytoprotective genes. RNA was isolated from the colons of untreated, PBS, E. coli, and LGG innoculated germ free mice and RNA-seq performed to identify the gene expression in response to each condition

2015-09-01 | E-GEOD-72552 | biostudies-arrayexpress

Lactobacilli modulate epithelial cytoprotection through the Nrf2 pathway [Microarray]

2015-09-01 | GSE72553 | GEO

Lactobacilli modulate epithelial cytoprotection through the Nrf2 pathway [RNA-Seq]

2015-09-01 | GSE72552 | GEO

Drosophila melanogaster

Project description:Lactobacilli modulate epithelial cytoprotection through the Nrf2 pathway [Microarray]

| PRJNA294322 | ENA

Mus musculus

Project description:Lactobacilli modulate epithelial cytoprotection through the Nrf2 pathway [RNA-Seq]

| PRJNA294323 | ENA

Lactobacilli Modulate Epithelial Cytoprotection through the Nrf2 Pathway.

Project description:An optimal gut microbiota influences many beneficial processes in the metazoan host. However, the molecular mechanisms that mediate and function in symbiont-induced host responses have not yet been fully characterized. Here, we report that cellular ROS enzymatically generated in response to contact with lactobacilli in both mice and Drosophila has salutary effects against exogenous insults to the intestinal epithelium via the activation of Nrf2 responsive cytoprotective genes. These data show that the xenobiotic-inducible Nrf2 pathway participates as a signaling conduit between the prokaryotic symbiont and the eukaryotic host. Indeed, our data imply that the capacity of lactobacilli to induce redox signaling in epithelial cells is a highly conserved hormetic adaptation to impel cellular conditioning to exogenous biotic stimuli. These data also highlight the role the microbiota plays in eukaryotic cytoprotective pathways and may have significant implications in the characterization of a eubiotic microbiota.

| S-EPMC4640184 | biostudies-literature

Lactobacilli modulate epithelial cytoprotection through the Nrf2 pathway

Project description:This SuperSeries is composed of the SubSeries listed below.

2015-09-01 | GSE70715 | GEO

Differential Targeting of the E-Cadherin and b-Catenin Complex by Gram-positive Probiotic Lactobacilli Improves Epithelial Barrier Function

Project description:The intestinal ecosystem is balanced by dynamic interactions between resident and incoming microbes, the gastrointestinal barrier, and the mucosal immune system. However, in the context of inflammatory bowel diseases (IBD) where the integrity of the gastrointestinal barrier is compromised, resident microbes contribute to the development and perpetuation of inflammation and disease. In this context, probiotic bacteria exert beneficial effects enhancing epithelial barrier integrity. However, the mechanisms underlying these beneficial effects are only poorly understood. Here, we comparatively investigated the effects of four probiotic lactobacilli, namely L. acidophilus, L. fermentum, L. gasseri, and L. rhamnosus in a T84 cell epithelial barrier model. Results of DNA-microarray experiments indicating that lactobacilli modulate the regulation of genes encoding in particular adherence junction proteins such as E-cadherin and b-catenin were confirmed by qRT-PCR. Furthermore, we show that epithelial barrier function is modulated by Gram-positive probiotic lactobacilli via their effect on adherence junction protein expression and complex formation. In addition, incubation with lactobacilli differentially influences the phosphorylation of adherence junction proteins and of PKC isoforms such as PKCd which thereby positively modulates epithelial barrier function. Further insight into the underlying molecular mechanisms triggered by these probiotics might also foster the development of novel strategies for the treatment of gastrointestinal diseases (e.g. IBD).

2012-02-10 | E-MEXP-3445 | biostudies-arrayexpress

Nrf2 transcript alterations

Project description:WGS and RNA-seq data for Nrf2 study

| EGAS00001001740 | EGA

The Prostacyclin Receptor is a Nrf2-regulated Immune Checkpoint in CD8+ T cells

Project description:Understanding how circulating metabolites enforce pathways in dysfunctional immune cells may illuminate modes of intervention directed at reviving immune function. The NRF2 pathway is the most widely documented cytoprotective axis in land-dwelling eukaryotes. However, the role of this pathway in CD8+ T cells—which seek and destroy tumors and pathogen infected cells—has yet to be elucidated. Our lab has conducted a RNAseq meta-analysis of CD8+ T cells upon tumor, viral and bacterial inoculation. Curiously, the NRF2 pathway was robustly upregulated in dysfunctional CD8+T cells. To further investigate the role of NRF2 in these contexts we developed a mouse model whereby the NRF2 axis is permanently hyperactivated in CD8+ T cells, hereafter referred to as NRF2Hi. Our in vivo data demonstrate that NRF2Hi CD8+ T cells offer little overall cytoprotection and poorly control tumors and pathogens versus wildtype (WT) control CD8+ T cells. To understand why upregulation of the NRF2 axis could be unfavorable to CD8+ T cell function we conducted RNAseq on NRF2Hi versus WT cells upon viral infection of mice. We found that NRF2Hi cells massively upregulate the prostacyclin receptor (PTGIR), which binds to prostacyclin—a circulating metabolite of arachidonic acid that has only been investigated in vasodilation and is seemingly benign to CD8+ T cells. To decipher the role of PTGIR in CD8+ T cells, we silenced its expression and observed a revival of CD8+ T cell function, significantly reducing tumor and pathogen burden. Collectively, our data illuminate a NRF2-regulated immune checkpoint, PTGIR. Interventions that suppress the interaction between PTGIR and prostacyclin may serve therapeutic benefit in clinical contexts such as cancer and chronic pathogen infections.

2024-07-17 | GSE244465 | 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