Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Evaluation of different responses of the intestinal microbiota to a TNF-α mediated pro-inflammatory stimulus by the HTF-Microbi.Array

ABSTRACT: We developed a non-invasive ex vivo HT29 cell-based minimal model to fingerprint the mucosa-associated microbiota fraction in humans. HT29 cell-associated fractions were characterized by the universal phylogenetic array platform HTF-Microbi.Array, both in presence or in absence of a TNF-α-mediated pro-inflammatory stimulus.

ORGANISM(S): synthetic construct human gut metagenome

PROVIDER: GSE51177 | GEO | 2013/09/26

SECONDARY ACCESSION(S): PRJNA221526

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Evaluation of different responses of the intestinal microbiota to a TNF-M-NM-1 mediated pro-inflammatory stimulus by the HTF-Microbi.Array

Project description:We developed a non-invasive ex vivo HT29 cell-based minimal model to fingerprint the mucosa-associated microbiota fraction in humans. HT29 cell-associated fractions were characterized by the universal phylogenetic array platform HTF-Microbi.Array, both in presence or in absence of a TNF-M-NM-1-mediated pro-inflammatory stimulus. A high taxonomical level fingerprint profiling of the mucosa-associated microbiota was performed on a group of 12 breast-fed infants and 6 adults (used as controls). Relative abundance of the bacterial species was assessed by using a so-called HTF-Microbi.Array, based on a ligation detection reaction (LDR) - Univerasal array (UA) assay, capable of correctly identify up to 31 intestinal bacterial groups, covering up to 95% of the human gut microbiota

2013-09-26 | E-GEOD-51177 | biostudies-arrayexpress

The enterocyte-associated intestinal microbiota of breast-fed infants and adults responds differently to a TNF-?-mediated pro-inflammatory stimulus.

Project description: Not available

| S-EPMC3841132 | biostudies-literature

Tonic TNF conditioning of macrophages safeguards stimulus-specific inflammatory responses

Project description:TNF is a key inflammatory cytokine that warns recipient cells of a nearby infection or tissue damage. Acute exposure to TNF activates characteristic oscillatory dynamics of the transcription factor NFκB and induces a characteristic gene expression program; these are distinct from the responses of cells directly exposed to pathogen-associated molecular patterns (PAMPs). Here we report that tonic TNF exposure is critical for safeguarding TNF’s specific functions. In the absence of tonic TNF conditioning, acute exposure to TNF causes 1) NFκB signaling dynamics that are less oscillatory and more like PAMP-responsive NFκB dynamics, 2) immune gene expression that is more similar to the Pam3CSK4-response program, 3) broader epigenomic reprogramming that is characteristic of PAMP-responsive changes. We show that tonic TNF signaling effects subtle changes to TNF receptor availability and dynamics such that enhanced pathway activity results in non-oscillatory NFκB. Our results reveal tonic TNF signaling as a key tissue determinant of the specific characteristics of cellular responses to acute paracrine TNF exposure, and their distinction from responses to direct exposure to PAMPs.

2022-07-27 | GSE209565 | GEO

Tonic TNF conditioning of macrophages safeguards stimulus-specific inflammatory responses

Project description: Not available

| S-SCDT-10_15252-EMBR_202255986 | biostudies-other

Colon cancer - Characterization of changes in the proteome in different regions of 3D multicell tumor spheroids

Project description:Proteins were extracted from different regions of HT29 colon carcinoma cells grown as multicell tumour spheroids. Changes in protein expression across the regions were determined by trypsin digestion iTRAQ 4-plex labelling, 2D separation using OffGel (24 fractions) and RP nanoHPLC, MALDI TOF-TOF MS/MS analysis and Mascot database searching.

2014-04-08 | PRD000369 | Pride

Umbilical cord blood methylome analysis of IVF neonates that underwent embryo culture in G5 or HTF medium

Project description:Follow-up study of IVF neonates who underwent embryo culture in G5 (Vitrolife) or HTF (Lonza) medium. Genome-wide DNA methylation profiling of IVF neonates (umbilical cord blood samples) who had undergone embryo culture in G5 medium (Vitrolife) or HTF medium (Lonza). The EPIC array was used to profile the methylome at approximately 850,000 CpG sites across the human genome.

2022-05-26 | GSE189531 | GEO

Mouse Sirt6-/- TNF-alpha timecourse

Project description:We completed genome-wide microarray analysis in Sirt6 knockout (ko) mouse embryonic fibroblasts (MEFs) and control wildtype (wt) MEFs. Prior to RNA extraction, MEFs were treated with TNF-alpha (10 ng/ml) for the indicated times. Total RNA was extracted with TRIzol (Invitrogen) and amplified with Ambion Amino Allyl MessageAmp II Amplification kit. Amplified mouse Universal Reference RNA (Stratagene) was used as reference RNA for analysis. Array hybridization of mouse MEEBO arrays is as described (Hendrickson et al., PLoS ONE, 2008). Groups of assays that are related as part of a time series. Compound Based Treatment: 10 ng/ml TNF-alpha Keywords: time_series_design

2009-01-09 | GSE13207 | GEO

TNF dependent induction of inhibitory pathways in CD4+ T cells in HIV and LCMV [TNF stimulation]

Project description:Chronic viral infections caused by HIV in humans or LCMV in mice are characterized by immunodeficiency and chronic inflammation. During chronification, T cells progressively lose effector functions, a process associated with immunoregulatory pathways and known as T-cell exhaustion. A link between ‘exhaustive’ T-cell reprogramming and chronic inflammation has not been established. Using a systems biology approach we demonstrate in HIV and LCMV infection that TNF, a prototypical mediator of chronic inflammation, functions upstream of major immunoregulatory pathways in T cells during chronic viral infection. In vivo blockade of TNFR-signaling interferes with the exhaustive T-cell program during chronic infection and reduces viral loads by several log. Continuous TNFR-signaling during disease progression towards chronic infection seems to be causative for T-cell exhaustion and an important link between immunodeficiency and chronic inflammation. TNF blockade might represent a novel therapeutic option during late stage infections caused by HIV and other virus causing chronic infections. TNF stimulation of CD4+ T cells to generate a CD4+ T-cell specific RNA-fingerprint

2016-03-07 | GSE52182 | GEO

Mutant p53 cancers reprogram macrophages to tumor supporting macrophages via exosomal miR-1246

Project description:exosomes isolated from: HT29+control shRNA; HT29+p53 shRNA; HCT116 WT p53; HCT116 mutant p53; HCT116 null p53; media used as negative control

2018-02-09 | MSV000082047 | MassIVE

Human shSIRT6 TNF-alpha timecourse

Project description:We established HeLa cell lines stably expressing a short hairpin RNA against SIRT6 (S6 sh2), and then completed genome-wide microarray analysis in shSIRT6 knock-down and control pSR HeLa cells. Prior to RNA extraction, HeLa cells were treated with TNF-alpha (5 ng/ml) for the indicated times. Total RNA was extracted with TRIzol (Invitrogen) and amplified with Ambion MessageAmp RNA Amplification kit. Amplified human Universal Reference RNA (Stratagene) was used as reference RNA for analysis. Construction and array hybridization of human cDNA microarrays were performed as previously described (Perou et al., 2000). Groups of assays that are related as part of a time series. Compound Based Treatment: 5 ng/ml TNF-alpha Keywords: time_series_design

2009-01-09 | GSE13206 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

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