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Gastrointestinal B-cells license metabolic T-cell activation in NASH microbiota anigen-independently and contribute to fibrosis by IgA-FcRy signalling

ABSTRACT: Gastrointestinal B-cells license metabolic T-cell activation in NASH microbiota anigen-independently and contribute to fibrosis by IgA-FcRy signalling

PROVIDER: PRJNA787280 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17171630_1.fastq.gz	Fastqsanger.gz
	SRR17171630_2.fastq.gz	Fastqsanger.gz

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Gastrointestinal B-cells license metabolic T-cell activation in NASH microbiota anigen-independently and contribute to fibrosis by IgA-FcRy signalling

Project description:Non-alcoholic steatohepatitis (NASH) is a T-cell mediated, auto-aggressive condition that can result in progressive liver disease and hepatocellular carcinoma. Gastrointestinal B-cells are activated and increased in number in mouse and human NASH, licensing metabolic-cell activation to induce NASH antigen- and microbiota-independently. Genetic or therapeutic depletion of B-cells systemically or gastrointestinal B-cells specifically prevented or reverted NASH and fibrosis. Clinical and molecular analyses from NASH patients demonstrated IgA-levels and activated FcRy+ hepatic myeloid cells to correlate with liver fibrosis degree.

2022-02-01 | GSE190487 | GEO

Intestinal B cells license metabolic T-cell activation in NASH microbiota/antigen-independently and contribute to fibrosis by IgA-FcR signalling

Project description:Non-alcoholic steatohepatitis (NASH), which is increasing in incidence due to the obesity epidemic, is a T-cell mediated, auto-aggressive condition that can result in progressive liver disease and hepatocellular carcinoma (HCC). The gut-liver axis contributes to NASH, yet mechanisms underlying metabolic T-cell activation and NASH-related fibrosis have largely remained elusive. We found that gastrointestinal B-cells are activated and increased in number in mouse/human NASH, allowing metabolic T-cell activation to induce NASH antigen- and microbiota-independently. Genetic/therapeutic depletion of B-cells systemically or of gastrointestinal B-cells specifically, prevented or reverted NASH and fibrosis. Secretion of immunoglobulins was essential for NASH and fibrosis development. IgA secretion was necessary for fibrosis-induction by activating CD11b+CCR2+F4/80+CD11c-FCGR1+ hepatic myeloid cells through an IgA-FcRγ signaling-axis. Furthermore, clinical/molecular analyses from NASH-patients demonstrated IgA and activated FcRγ+ hepatic myeloid cells to correlate with the degree of liver-fibrosis. Thus, gastrointestinal B-cells and the IgA-FcRγ signaling-axis on hepatic myeloid cells represent potential therapeutic targets to treat NASH.

2023-11-22 | GSE190204 | GEO

Gastrointestinal B-cells license metabolic T-cell activation in NASH microbiota/antigen-independently and contribute to fibrosis by IgA-FcRγ signaling

Project description:Gastrointestinal B-cells license metabolic T-cell activation in NASH microbiota/antigen-independently and contribute to fibrosis by IgA-FcRγ signaling

| PRJNA787962 | ENA

Intestinal B cells license metabolic T-cell activation in NASH microbiota/antigen-independently and contribute to fibrosis by IgA-FcR signalling

Project description:Intestinal B cells license metabolic T-cell activation in NASH microbiota/antigen-independently and contribute to fibrosis by IgA-FcR signalling

| PRJNA786336 | ENA

Gastrointestinal B-cells license metabolic T-cell activation in NASH microbiota/antigen-independently and contribute to fibrosis by IgA-FcRγ signaling

Project description:Purpose: Aim of the study was to identify transcriptional changes in the intestinal B cells of NASH-affected mice versus healthy mice. Results: RNA-Seq analysis in both sorted CD19+/CD20+ and sorted B220+ cells, revealed increased expression levels in genes involved in lipid metabolism, and in antigen presentation, BCR signaling, B cells activation and proliferation. Conclusion: Mice bearing NASH (both WT and μMT choline-deficient high-fat diet (CD-HFD) fed mice) display altered B cells in the gastrointestinal tract towards an activated phenotype and increased proliferation induced by the CD-HFD.

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Intestinal B cells license metabolic T-cell activation in NASH microbiota/antigen-independently and contribute to fibrosis by IgA-FcR signalling.

Project description: Not available

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NASH

Project description:Non-alcoholic fatty liver disease (NAFLD) is characterized by a series of pathological changes that can progress from simple fatty liver disease to non-alcoholic steatohepatitis (NASH). The objective of this study is to describe changes in global gene expression associated with the progression of NAFLD. This study is focused on the expression levels of genes responsible for the absorption, distribution, metabolism and excretion (ADME) of drugs. Differential gene expression between three clinically defined pathological groups; normal, steatosis and NASH was analyzed. The samples were diagnosed as normal, steatotic, NASH with fatty liver (NASH fatty) and NASH without fatty liver (NASH NF). Genome-wide mRNA levels in samples of human liver tissue were assayed with Affymetrix GeneChipM-. Human 1.0ST arrays

2011-07-12 | E-MEXP-3291 | biostudies-arrayexpress

A Metabolic Switch Controlling Liver Cancer Evolution from Senescent NASH Hepatocytes

Project description:Hepatocellular carcinoma (HCC), the third most common cancer, originates from differentiated hepatocytes undergoing compensatory proliferation in livers damaged primarily by viruses or nonalcoholic steatohepatitis (NASH)1,2. While increasing HCC risk3, NASH also induces TP53-dependent hepatocyte senescence4. How this tumor-suppressive response is activated but eventually bypassed to license HCC progression is unknown. We identified the gluconeogenic enzyme fructose-1,6-bisphosphatase 1 (FBP1) as a TP53 target, induced in senescent NASH hepatocytes but downregulated in most human HCCs. Initial FBP1 downregulation in disease-associated hepatocytes, whose accumulation precedes HCC development5, activates AKT to inhibits GSK3 substrate binding, thereby augmenting activation of NRF2 which accelerates FBP1 and TP53 degradation. Intrinsic NRF2 activation and FBP1 loss trigger overlapping transcriptomic responses that suppress senescence, enhance hepatocyte proliferation and metabolism, and enable NRAS- or NASH-induced hepatocarcinogenesis. This AKT-dependent metabolic switch, operative in mice and humans, controls NASH to HCC progression. Our results further suggest that NASH-related hepatocyte senescence is triggered by hypernutrition-induced single strand DNA breaks. Senescence reversal enables HCC progenitor expansion and somatic mutagenesis.

2024-07-15 | GSE240047 | GEO

A Metabolic Switch Controlling Liver Cancer Evolution from Senescent NASH Hepatocytes

Project description:Hepatocellular carcinoma (HCC) originates from differentiated hepatocytes undergoing compensatory proliferation in livers damaged by viruses or nonalcoholic steatohepatitis (NASH). While increasing HCC risk, NASH triggers TP53-dependent hepatocyte senescence, which we found to parallel hypernutrition-induced DNA breaks. How this tumor-suppressive response is bypassed to license accumulation of oncogenic mutations and enable HCC progression was previously unknown. We identified the gluconeogenic enzyme fructose-1,6-bisphosphatase 1 (FBP1) as a TP53 target that is elevated in senescent-like NASH hepatocytes but suppressed through promoter hypermethylation and proteasomal degradation in most human HCCs. FBP1 first declines in metabolically-stressed premalignant disease-associated hepatocytes and HCC progenitor cells, paralleling the protumorigenic activation of AKT and NRF2. By accelerating FBP1 and TP53 degradation AKT and NRF2 enhance the proliferation and metabolic activity of previously senescent HCC progenitors. The senescence-reversing NRF2-FBP1-AKT-TP53 metabolic switch, operative in mice and humans, also enhances proliferation-enabled accumulation of DNA damage-induced somatic mutations that drive NASH to HCC progression.

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Gene expression on CD11b+ IgA and CD11b- IgA cells in the small intestine #01

Project description:To compare gene expression between CD11b+ IgA and CD11b- IgA cells in the small intestine, each cell population was isolated from the murine small intestine. Similar experiment with different sample was performed as described in Gene expression on CD11b+ IgA and CD11b- IgA cells in the small intestine #02

2013-04-01 | E-GEOD-37225 | biostudies-arrayexpress

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