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Synbiotic-Derived Metabolites Alleviate Stress-Induced Depression by Regulating Lymphocyte Activation through the Aryl Hydrocarbon Receptor

ABSTRACT: Synbiotic-Derived Metabolites Alleviate Stress-Induced Depression by Regulating Lymphocyte Activation through the Aryl Hydrocarbon Receptor

PROVIDER: PRJNA625073 | ENA |

REPOSITORIES: ENA

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Synbiotic-Derived Metabolites Alleviate Stress-Induced Depression by Regulating Lymphocyte Activation through the Aryl Hydrocarbon Receptor

Project description:Synbiotics are a combination of probiotics and prebiotics which can alter the composition of the gastrointestinal tract evoking beneficial effects throughout the body through the production of a battery of bioactive metabolites. In this study, a synbiotic was used to reduce the behavioral and biochemical symptoms of depression and this nanostring panel was used to decipher where along the gut-brain-axis the synbiotic-derived metabolites were invoking their beneficial effects on the immune system. The synbitoic was composed of two probiotic bacteria (Lactobacillus fermentum ATCC 793 and Bifidobacteria longum ATCC 15707 and a grape -derived prebiotic composed of grape seed polyphenol extract, resveratrol and a concord grape extract. Male mice (C57BL/6) were pretreatment with either nothing (control), BDPP, probiotic or synbiotic and underwent 28 days of chronic unpredicitable stress. After 28 days, animals' behavior reflected an increase in depressive- and anxiety-like behavior, rescued specifically by the synbiotic. This nanostring multiplex analysis reveals both tissue- and treatment-specific effects on immune modulators.

2020-11-03 | GSE148579 | GEO

The Aryl Hydrocarbon Receptor Regulates Tissue-Specific Dioxin-Dependent and Dioxin-Independent Gene Batteries

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2010-05-05 | E-GEOD-15859 | biostudies-arrayexpress

Activation of aryl hydrocarbon receptor

Project description:VAF347 is a low molecular weight compound which inhibits allergic lung inflammation in vivo. This effect is likely due to a block of dendritic cell (DC) function to generate pro-inflammatory T-helper (Th) cells since VAF347 inhibits IL-6, CD86 and HLA-DR expression by human monocyte derived DC, three relevant molecules for Th-cell generation. Here we demonstrate that VAF347 interacts with the aryl hydrocarbon receptor (AhR) protein resulting in activation of the AhR signaling pathway. Functional AhR is responsible for the biological activity of VAF347 since, i) other AhR agonists display an identical activity profile in vitro, ii) gene silencing of wild type AhR expression or forced over-expression of a trans-dominant negative AhR ablates VAF347 activity to inhibit cytokine induced IL-6 expression in a human monocytic cell line and iii) AhR deficient mice are resistant to the compound’s ability to block allergic lung inflammation in vivo. These data identify the AhR protein as key molecular target of VAF347 and its essential role for mediating the anti-inflammatory effects of the compound in vitro and in vivo. Keywords: effect of compound

2008-02-12 | GSE10463 | GEO

The Aryl hydrocarbon receptor and FOS mediated cytotoxicity induced by Acenatobacter baumannii

Project description:Acinetobacter baumannii is a highly pathogenic and multidrug-resistant Gram-negative bacterium that causes severe nosocomial infections. To better understand the mechanism of pathogenesis, we compare the proteomes of uninfected and infected human cells, revealing that transcription factor FOS is the host protein most strongly induced by A. baumannii infection. Pharmacological inhibition of FOS reduces the cytotoxicity of A. baumannii in cell-based models, and similar results are also observed in a mouse infection model. A. baumannii outer membrane vesicles (OMVs) are shown to activate the aryl hydrocarbon receptor (AHR) of host cells by inducing the host enzyme tryptophan-2,3-dioxygenase (TDO), producing the ligand kynurenine, which binds AHR. Following ligand binding, AHR is a direct transcriptional activator of the FOS gene. Our results suggest that bacterial infection interacts with host tryptophan metabolism and the transcription factor FOS.

2024-08-05 | PXD053768 | Pride

Aryl hydrocarbon receptor-interacting protein regulates tumorigenic and metastatic properties of colorectal cancer cells driving liver metastasis

Project description:Aryl hydrocarbon receptor-interacting protein (AIP), a putative positive intermediary in aryl hydrocarbon receptor-mediated signaling, is overexpressed in highly metastatic human KM12SM CRC cells, with high metastatic capacity to liver, and other highly metastatic CRC cells. Meta-analysis and immunohistochemistry were used to assess the relevance of this protein in CRC. Cellular functions and signaling mechanisms mediated by AIP were assessed by gain-of-function experiments and in vitro and in vivo experiments. A significant association of high AIP expression with poor CRC patients’ survival was observed. Gain-of-function and quantitative proteomics experiments demonstrated that AIP increased tumorigenic and metastatic properties of isogenic KM12C (poorly-metastatic) and KM12SM CRC cells. AIP overexpression dysregulated epithelial-to-mesenchymal (EMT) markers and induced several transcription factors and Cadherin-17 activation. The former induced the signaling activation of AKT, SRC, and JNK kinases to increase adhesion, migration and invasion of CRC cells. In vivo, AIP expressing KM12 cells induced tumor growth and liver metastasis. Furthermore, KM12C (poorly-metastatic) cells ectopically expressing AIP became metastatic to liver. Our data reveal new roles for AIP in regulating proteins associated with cancer and metastasis to induce tumorigenic and metastatic properties in colon cancer cells driving liver metastasis.

2023-05-10 | PXD031119 | Pride

Zebrafish larvae aryl hydrocarbon receptor ligands and inhibitor

Project description:Zebrafish larvae aryl hydrocarbon receptor ligands and inhibitor

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Aryl hydrocarbon receptor dynamically regulates inflammatory and secretory gene pathways in decidual endometrial stromal cells

Project description:We report sequencing of chromatin immunoprecipitated DNA (ChIP-Seq) of Aryl Hydrocarbon Receptor (AHR) targets from decidual stromal cells with kynurenine treatment and normal decidualization media

2019-06-01 | GSE118413 | GEO

Effect of canonical aryl hydrocarbon receptor pathway inhibitor on human umbilical vein endothelial cells

Project description:To study the effect of blockade of canonical aryl hydrocarbon receptor (AHR) pathway in human endothelial cells, we treated human umbilical vein endothelial cells (HUVECs) with a canonical AHR inhibitor, Stemreginin 1 (SR1) and performed bulk RNAseq analysis.

2024-07-01 | GSE251861 | GEO

Aryl Hydrocarbon Receptor deficiency influences B cell response

Project description:The aryl hydrocarbon receptor (AhR), a transcription factor known for mediating xenobiotic toxicity, is expressed in B cells, which are known targets for environmental pollutants. However, it is unclear what the physiological functions of AhR in B cells are. We show here that expression of Ahr in B cells is up-regulated upon B cell receptor (BCR) engagement and IL-4 treatment. Addition of a natural ligand of AhR, FICZ, induces AhR translocation to the nucleus and transcription of the AhR target gene Cyp1a1, showing that the AhR pathway is functional in B cells. AhR-deficient (Ahr-/-) B cells proliferate less than AhR-sufficient (Ahr+/+) cells following in vitro BCR stimulation and in vivo adoptive transfer models confirmed that Ahr-/- B cells are outcompeted by Ahr+/+ cells. Transcriptome comparison of AhR-deficient and sufficient B cells identified cyclin O (Ccno), a direct target of AhR, as a top candidate affected by AhR deficiency.

2016-11-16 | GSE86521 | GEO

Aryl hydrocarbon receptor dynamically regulates immunological and secretory gene pathways in decidual endometrial stromal cells

Project description:We report mRNA sequencing from decidual stromal cells after 24 hours and 6 days treatment with Aryl Hydrocarbon Receptor (AHR) activators 100 µM L-kynurenine or 10 nM TCDD (2,3,7,8-Tetrachlorodibenzo-p-dioxin)

2019-06-01 | GSE114552 | GEO

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