Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Intestinal alcohol abuse sorted dendritic cells proteomics

ABSTRACT: Consumption of ethanol has detrimental effects on gastric organs such as the intestine. To demonstrate the deleterious effect of alcohol, we sacrificed isobaric feeding or ethanol feeding mice and sorted the dendritic cells from their intestine organ. The dendritic cells were analyzed by a small-scale global proteomics approach. We achieved to obtain the biological signatures in the alcohol abuse mice group using bioinformatics analysis.

INSTRUMENT(S): Orbitrap Exploris 240

ORGANISM(S): Mus Musculus (mouse)

TISSUE(S): Diploid Cell, Small Intestine

DISEASE(S): Alcohol

SUBMITTER: Qibin Zhang

LAB HEAD: Jongmin Woo

PROVIDER: PXD033700 | Pride | 2024-06-16

REPOSITORIES: pride

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	072221_60SPD_DCs_200ng_Sample_01.raw	Raw
	072221_60SPD_DCs_200ng_Sample_02.raw	Raw
	072221_60SPD_DCs_200ng_Sample_03.raw	Raw
	072221_60SPD_DCs_200ng_Sample_04.raw	Raw
	072221_60SPD_DCs_200ng_Sample_05.raw	Raw

Items per page:

1 - 5 of 19

Publications

Conventional type 1 dendritic cells protect against gut barrier disruption via maintaining Akkermansia muciniphila in alcoholic steatohepatitis.

Hao Liuyi L Zhong Wei W Woo Jongmin J Wei Xiaoyuan X Ma Hao H Dong Haibo H Guo Wei W Sun Xinguo X Yue Ruichao R Zhao Jiangchao J Zhang Qibin Q Zhou Zhanxiang Z

Hepatology (Baltimore, Md.) 20230103 3

<h4>Background and aims</h4>Alcohol-perturbed gut immune homeostasis is associated with the development of alcoholic liver disease (ALD). However, the role of intestinal dendritic cells (DCs) in ALD progression is still unknown. This study aimed to investigate the cellular and molecular mechanisms through which intestinal DCs respond to alcohol exposure and contribute to the pathogenesis of ALD.<h4>Approach and results</h4>After 8 weeks of alcohol consumption, the number of basic leucine zipper ...[more]

PMID: 36626632

Similar Datasets

Microglia depletion and alcohol: Transcriptome and behavioral

Project description:Purpose: Alcohol abuse induces changes in microglia morphology and immune function, but whether microglia initiate or simply amplify the harmful effects of alcohol exposure is still a matter of debate. Here we determined microglia function in acute and voluntary drinking behaviors using a colony stimulating factor 1 receptor inhibitor (PLX5622) and 3’UTR biased-sequencing. Therefore, The purpose of this study was to provide insight regarding microglia depletion and voluntary alcohol consumption. Methods: We performed 3’UTR biased transcriptome sequencing (3’Tag-seq) on total homogenate isolated from the prefrontal cortex (PFC) of C57BL6/J mice following microglia depletion and chronic every-other-day alcohol consumption. Results: Differential expression analysis and WGCNA network analysis revealed that although many immune genes have been implicated in alcohol abuse, downregulation of microglia genes does not necessitate changes in alcohol intake. Finally, we show that microglia depletion and chronic alcohol result in compensatory upregulation of ethanol-responsive, reactive astrocyte genes, indicating astrocytes may play a critical role in regulation of these alcohol behaviors. Conclusion:Taken together our behavioral and transcriptional data indicate that microglia are not the primary effector cell responsible for regulation of acute and voluntary alcohol behaviors. In addition, our data represents a novel resource for groups interested in transcriptional effects of microglia depletion after alcohol consumption.

2020-06-01 | GSE132516 | GEO

Gene expression in the human VTA of cases with alcohol abuse

Project description:Drugs of abuse including nicotine and alcohol elicit their effect by stimulating the mesocorticolimbic dopaminergic system. There is a high incidence of nicotine dependence in alcoholics. To date only limited data is available on the molecular mechanism underlying the action of alcohol and nicotine in the human brain. This study utilised gene expression screening to identify genes sensitive to chronic alcohol abuse within the ventral tegmental area of the human brain. Keywords: gene expression, brain, alcohol abuse, human, ventral tegmental area

2007-09-21 | GSE9058 | GEO

Distinct Metabolic Adaptation of Liver Circadian Pathways to Acute and Chronic Patterns of Alcohol Intake

Project description:We reveal differential reprogramming of the circadian transcriptome in the liver using acute versus chronic ethanol feeding. Specifically, rewiring of diurnal SREBP transcriptional pathway leads to distinct hepatic signatures in acetyl-CoA metabolism that are translated into the subcellular patterns of protein acetylation distinct to chronic exposure to ethanol. Therefore, distinct drinking patterns of alcohol result in differential circadian reprogramming that may contribute to ALD pathogenesis.

2019-11-30 | GSE132103 | GEO

Deep sequencing and miRNA profiles in alcohol-induced neuroinflammation and the TLR4 response in mice cerebral cortex

Project description:Alcohol abuse can induce brain injury and neurodegeneration, and recent evidence shows the participation of immune receptors toll-like in the neuroinflammation and brain damage. We evaluated the role of miRNAs as potential modulators of the neuroinflammation associated with alcohol abuse and the influence of the TLR4 response. Using mice cerebral cortex and next-generation sequencing (NGS), we identified miRNAs that were differentially expressed in the chronic alcohol-treated versus untreated WT or TLR4-KO mice. We observed a differentially expression of miR-183 Cluster (C) (miR-96/-182/-183), miR-200a and miR-200b, which were down-regulated, while mirR-125b was up-regulated in alcohol-treated WT versus (vs.) untreated mice. These miRNAs modulate targets genes related to the voltage-gated sodium channel, neuron hyperexcitability (Nav1.3, Trpv1, Smad3 and PP1-γ), as well as genes associated with innate immune TLR4 signaling response (Il1r1, Mapk14, Sirt1, Lrp6 and Bdnf). Functional enrichment of the miR-183C and miR-200a/b family target genes, revealed neuroinflammatory pathways networks involved in TLR4 signaling and alcohol abuse. The changes in the neuroinflammatory targets genes associated with alcohol abuse were mostly abolished in the TLR4-KO mice. Our results show the relationship between alcohol intake and miRNAs expression and open up new therapeutically targets to prevent deleterious effects of alcohol on the brain.

2018-09-25 | GSE120373 | GEO

Candida albicans-specific Th17 cell-mediated response contributes to alcohol-associated liver disease [bulk TCR-seq]

Project description:Alcohol-associated liver disease is accompanied by changes in the intestinal mycobiome. How fungal dysbiosis contributes to liver disease is not clear. T-helper (Th17) cells mediate immune responses against fungi, but the interleukin 17 (IL17) pathway has been associated with pathogenesis of alcohol-associated liver disease. Here, we demonstrate that Candida albicans (C. albicans)-specific Th17 cells are increased in the circulation and present in the liver of patients with alcohol-associated liver disease. Chronic ethanol administration to mice results in migration of C. albicans-reactive Th17 cells from the intestine to the liver. The antifungal agent nystatin reduced intestinal fungal overgrowth, decreased C. albicans-specific Th17 cells in the liver, and reduced features of ethanol-induced liver disease in mice. Transgenic mice that express a T-cell receptor (TCR) reactive to Candida antigens develop more severe ethanol-induced liver disease than transgene-negative littermates; disease severity was reduced by administration of an antibody against IL17 to the TCR transgenic mice. Adoptive transfer of C. albicans-reactive Th17 cells exacerbated ethanol-induced liver disease in wild-type mice. IL17 receptor A (IL17ra) signaling in Kupffer cells was required for the effects of C. albicans-reactive Th17 cells. Our findings indicate that ethanol increases C. albicans-reactive Th17 cells, which contribute to alcohol-associated liver disease.

2023-02-16 | GSE215929 | GEO

Candida albicans-specific Th17 cell-mediated response contributes to alcohol-associated liver disease [scRNA & scTCR-seq]

2023-02-16 | GSE215930 | GEO

Blockade of lL17 signaling reverses alcohol-induced liver injury, and excessive alcohol drinking in mice.

Project description:Chronic alcohol abuse has a detrimental effect on the brain and liver. There is no effective treatment for these patients and the mechanism underlying alcohol addiction and consequent alcohol-induced damage of the liver/brain axis remains unresolved. We compared experimental models of alcoholic liver disease (ALD) and alcohol dependence in mice and demonstrated that genetic ablation of IL17 Receptor A (IL17ra-/-), or pharmacological blockade of IL17 signaling effectively suppressed the increased voluntary alcohol drinking in alcohol-dependent mice, and blocked alcohol-induced hepatocellular and neurological damage. The level of circulating IL17A positively correlated with the alcohol use in excessive drinkers, and was further increased in patients with ALD as compared to healthy individuals. Our data suggest that IL17A is a common mediator of excessive alcohol consumption and alcohol-induced liver/brain injury, and targeting IL17A may provide a novel strategy for treatment of alcohol-induced pathology.

2020-04-07 | GSE137228 | GEO

Chronic alcohol drinking compromises lung immunity by altering immunometabolism in both human and mouse lungs

Project description:Heavy alcohol drinking dysregulates lung immunity and host defense, which makes individuals with AUD more susceptible to develop inflammatory condition in lungs with poor prognosis. Current study, we focused on exploring the effects of chronic alcohol consumption on lungs using NIAAA alcohol feeding model in mice with 10 days of a Lieber-DeCarli liquid diet containing 5% ethanol followed by a single ethanol binge (5 g/kg) and population based human lung transcriptome data from Genotype-Tissue Expression (GTEx) project consist of 328 alcohol drinkers and 110 non-drinkers. Flow cytometry and transcriptomics analysis in mice lungs revealed that alcohol consumption dysregulates cellularity of immune cell levels and lung immunity. Transcriptomics analysis both in lungs and liver at 9-, 24- hours and 14 days post ethanol binge in mice uncovered that the lungs were more sensitive to alcohol effect to down-regulate pathways of immune system regulations than liver. Comparative data analysis of lung transcriptomes between mice and human subjects not only confirmed similar dysregulation on lung immunity but also provided evidence that immunometabolic changes are the central driver of alterations in lung transcriptome with down regulating immune pathways and upregulating metabolic pathways. Since the NIAAA model recapitulates multiple changes in the lung transcriptome that had been observed in human subjects with chronic alcohol drinking, this makes the mouse model suitable for experimental studies exploring role of alcohol drinking in lung health. Chronic alcohol drinking reduced mTOR signaling and cellularity of immune cells, which can be further attenuated by selective inhibition of mTOR. BCAA-mTOR signaling axis can be an upstream regulator of alcohol induced dysregulation in lung immunity

2024-07-22 | GSE248233 | GEO

Transcription profiling of Drosophila newly exposed to ethanol, tolerant of ethanol or untreated to investigate gene expression changes in response to alcohol reveals immediate down-regulation of olfactory sensitivity and altered transcription of enzymes associated with fatty acid biosynthesis

Project description:The National Institute on Alcohol Abuse and Alcoholism has estimated that approximately 14 million people in the United States suffer from alcoholism. Alcohol sensitivity, the development of tolerance to alcohol and susceptibility to addiction vary in the population. Whereas environmental factors, such as stress and social experience, contribute to individual variation in sensitivity to chronic alcohol consumption, genetic factors have also been implicated. However, genetic polymorphisms that predispose to alcoholism remain largely unknown due to extensive genetic and environmental variation in human populations. Drosophila, however, allows studies on genetically identical individuals in controlled environments. Although addiction to alcohol has not been demonstrated in Drosophila, flies show responses to alcohol exposure that resemble human intoxication, including hyperactivity, loss of postural control, sedation, and exposure-dependent development of tolerance. We assessed whole-genome transcriptional responses following alcohol exposure and demonstrate immediate down-regulation of olfactory sensitivity and, concomitant with development of tolerance, altered transcription of enzymes associated with fatty acid biosynthesis. Our results identify key enzymes in conserved metabolic pathways that may contribute to human alcohol sensitivity. Experiment Overall Design: Alcohol sensitivity in Drosophila melanogaster can be quantified in an inebriometer. The elution time from the column is used as a measure of sensitivity to alcohol intoxication. Overall design: We collected 3-5 day old Canton S flies either without exposure to ethanol (control group), immediately after passage through the inebriometer, or from a population that had developed tolerance 2h after the initial ethanol exposure.

2008-03-13 | E-GEOD-5382 | biostudies-arrayexpress

Genes associated with alcohol abuse and nicotine addiction in the human nucleus accumbens

Project description:Background: The incidence of alcohol and tobacco co-abuse is as high as 80%. The molecular mechanism underlying this comorbidity is virtually unknown but interactions between these drugs have important implications for the development of, and recovery from drug dependence. Methods: We investigated the effects of chronic tobacco and alcohol abuse and the interaction of the two behaviours on global gene expression in the human nucleus accumbens using cDNA microarrays and 20 alcoholic and control cases, with and without smoking comorbidity. Changes in gene expression were established by two-way ANOVA. Unsupervised hierarchical clustering was utilized to probe the strength of the data sets. Results: Subjecting the data sets derived from microarray gene expression screening to unsupervised hierarchical clustering tied the cases into distinct groups. When considering all alcohol-responsive genes, alcoholics were separated from non alcoholics with the exception of one control case. All smokers were distinguished from non smokers based on similarity in expression of smoking-sensitive genes. In the nucleus accumbens, alcohol-responsive genes were associated with transcription, lipid metabolism and signalling. Smoking-sensitive genes were predominantly assigned to functional groups concerned with RNA processing and the endoplasmic reticulum. Both drugs influenced the expression of genes involved in matrix remodelling, proliferation and cell morphogenesis. Additionally, a gene set encoding proteins involved in the canonical pathway ‘regulation of the actin cytoskeleton’ was induced in response to alcohol and tobacco co-abuse and included. Conclusions: The region-specific modulation of alcohol-sensitive gene expression by smoking may have important consequences for alcohol-induced aberrations within the mesolimbic dopaminergic system.

2010-07-01 | GSE20568 | 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