Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Gut epithelial barrier damage caused by dishwasher detergents and rinse aids

ABSTRACT: We investigated the effects of professional dishwasher detergents and rinse aid on cytotoxicity, barrier function and the transcriptome in gastrointestinal epithelial cells. RNA-seq was used for checking transcriptome.

ORGANISM(S): Homo sapiens

PROVIDER: GSE203549 | GEO | 2022/05/25

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Gut epithelial barrier damage caused by dishwasher detergents and rinse aids

Project description:Gut epithelial barrier damage caused by dishwasher detergents and rinse aids

| PRJNA841364 | ENA

Mechanisms of gut epithelial barrier impairment caused by food emulsifiers polysorbate 20 and polysorbate 80

Project description:We investigated the effects of polysorbate 20 and polysorbate 80 on cytotoxicity, barrier function and the transcriptome in gastrointestinal epithelial cells. RNA-seq was used for checking transcriptome.

2023-03-25 | GSE227220 | GEO

Household laundry detergents disrupt barrier integrity and induce inflammation in mouse and human skin

Project description:To investigate the effect of household detergents on the mouse skin barrier, we treated mouse's back skin with two household detergents (A and B) and collected the treated skin 24 hours after the application. We then performed gene expression profiling analysis using data obtained from RNA-seq of mouse skin treated with detergent A, detergent B, and PBS. We performed gene expression profiling analysis using data obtained from RNA-seq of the skin biopsy at 24 hours after the application.

2023-10-03 | GSE234841 | GEO

Opioid-induced gut microbial disruption leads to gut barrier compromise and sustained systemic inflammation.

Project description:Morphine and its pharmacological derivatives are the most prescribed analgesics for moderate to severe pain management. However, chronic use of morphine reduces pathogen clearance and induces bacterial translocation across the gut barrier. The enteric microbiome has been shown to play a critical role in the preservation of the mucosal barrier function and metabolic homeostasis. Here, we show for the first time, using bacterial 16s rDNA sequencing, that chronic morphine treatment significantly alters the gut microbial composition and induces preferential expansion of the gram-positive pathogenic and reduction of bile-deconjugating bacterial strains. A significant reduction in both primary and secondary bile acid levels was seen in the gut, but not in the liver with morphine treatment. Morphine induced microbial dysbiosis and gut barrier disruption was rescued by transplanting placebo-treated microbiota into morphine-treated animals, indicating that microbiome modulation could be exploited as a therapeutic strategy for patients using morphine for pain management. In this study, we establish a link between the two phenomena, namely gut barrier compromise and dysregulated bile acid metabolism. We show for the first time that morphine fosters significant gut microbial dysbiosis and disrupts cholesterol/bile acid metabolism. Changes in the gut microbial composition is strongly correlated to disruption in host inflammatory homeostasis13,14 and in many diseases (e.g. cancer/HIV infection), persistent inflammation is known to aid and promote the progression of the primary morbidity. We show here that chronic morphine, gut microbial dysbiosis, disruption of cholesterol/bile acid metabolism and gut inflammation; have a linear correlation. This opens up the prospect of devising minimally invasive adjunct treatment strategies involving microbiome and bile acid modulation and thus bringing down morphine-mediated inflammation in the host.

2016-06-01 | E-MTAB-3722 | biostudies-arrayexpress

IP pTKL - Plasmodium pseudo-Tyrosine Kinase-like binds PP1 and SERA5 and is exported to host erythrocytes

Project description:PbpTKL-AID-HA was immunoprecipitated from iRBC ghosts at trophozoite stages and from parasite + PV fractions at schizont stages. Total lysis of P. berghei pG230 strain trophozoites was also performed and anti-HA immunoprecipitation assays were performed on lysates as for ghosts to generate WT samples. After checking by WB for the presence of PbpTKL-AID-HA in ghost and schizont samples, as well as its absence from WT samples, 3 biological replicates were analyzed by Mass Spectrometry for each sample.

2019-06-05 | PXD011986 | Pride

Novel DNA methylation targets in oral rinse samples predict survival of patients with oral squamous cell carcinoma

Project description:Epigenome-wide association study (EWAS) of oral rinse samples from a cohort of 82 oral squamous cell carcinoma (OSCC) patients. The Illumina Infinium HumanMethylation450 Beadchip was used to obtain DNA methylation profiles across approximately 450,000 CpGs in oral rinse samples. Bisulphite lsconverted DNA from the 82 oral rinse samples were hybridized to the Illumina Infinium HumanMethylation450 Beadchip

2014-11-25 | E-GEOD-52793 | biostudies-arrayexpress

Transcription profile of primordium gut organs

Project description:The mechanisms of gastrointestinal morphogenesis in mammals are not well understood. This is partly due to the lack of organ specific gene expression pattern in the gastrointestinal tract during development. The initiation of organ bud formation occurs at E9.5-E11.5 in mice. These primordia for the digestive organs, including esophagus, stomach, and intestine, protrude from a tube-like structured endoderm, and have their own distinct morphogenesis. Thus, using mouse embryos, we surveyed transcription of prospective these three regions at E11.5 during gastrointestinal morphogenesis. This early digestive organ specific transcription profile will be useful for understanding of the mechanisms of gastrointestinal development. Mouse gut organs morphogenesis begin at E9.5-E11.5. The primordium esophagus, stomach, and intestine at E11.5 were dissected and analysed transcription profile.

2012-05-31 | E-GEOD-30742 | biostudies-arrayexpress

Novel DNA methylation targets in oral rinse samples predict survival of patients with oral squamous cell carcinoma

2014-11-25 | GSE52793 | GEO

CpG island methylation profile in non-invasive oral rinse samples is predictive of oral and pharyngeal carcinoma

Project description:Epigenome-wide association study (EWAS) of oral rinse samples from a case-control study of 154 cases and 72 controls. The Illumina Infinium HumanMethylation450 Beadchip was used to obtain DNA methylation profiles across approximately 450,000 CpGs in oral rinse samples.

2016-07-13 | GSE70977 | GEO

Vitamin D Reverses Disruption of Gut Epithelial Barrier Function Caused by <i>Campylobacter jejuni</i>.

Project description:Infections by the zoonotic foodborne bacterium Campylobacter jejuni (C. jejuni) are among the most frequent causes of bacterial gastroenteritis worldwide. The aim was to evaluate the relationship between epithelial barrier disruption, mucosal immune activation, and vitamin D (VD) treatment during C. jejuni infection, using intestinal epithelial cells and mouse models focused on the interaction of C. jejuni with the VD signaling pathway and VD treatment to improve C. jejuni-induced barrier dysfunction. Our RNA-Seq data from campylobacteriosis patients demonstrate inhibition of VD receptor (VDR) downstream targets, consistent with suppression of immune function. Barrier-preserving effects of VD addition were identified in C. jejuni-infected epithelial cells and IL-10-/- mice. Furthermore, interference of C. jejuni with the VDR pathway was shown via VDR/retinoid X receptor (RXR) interaction. Paracellular leakiness of infected epithelia correlated with tight junction (TJ) protein redistribution off the TJ domain and apoptosis induction. Supplementation with VD reversed barrier impairment and prevented inhibition of the VDR pathway, as shown by restoration of transepithelial electrical resistance and fluorescein (332 Da) permeability. We conclude that VD treatment restores gut epithelial barrier functionality and decreases bacterial transmigration and might, therefore, be a promising compound for C. jejuni treatment in humans and animals.

| S-EPMC8396270 | biostudies-literature

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