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ABSTRACT: AKK blunts IBD

PROVIDER: PRJNA881950 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR21622540_1.fastq.gz	Fastqsanger.gz
	SRR21622540_2.fastq.gz	Fastqsanger.gz
	SRR21622541_1.fastq.gz	Fastqsanger.gz
	SRR21622541_2.fastq.gz	Fastqsanger.gz
	SRR21622542_1.fastq.gz	Fastqsanger.gz

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Akkermansia muciniphila reduces lipid absorption through activating AMPK in the jejunum

Project description:Akkermansia muciniphila (Akk) associated with multiple metabolic diseases and administration of Akk can improve the metabolic disorders. However, little is known about the effect of Akk on jejunal epithelial cells which absorb lipid and interact with oral administrated Akk. We oral administrated Akk to mice and measured the lipid absorption and gene expression in small intestinal epithelial cells. The long-term effect of Akk treatment reduced lipid deposits in the liver and adipocytes with improved the glucose metabolism. This is particularly caused by reduced lipid absorption in jejunal epithelia. Akk feeding reduced the expression of those genes that regulate synthesis and cell cycles, characters of the host cell responding to energy deficiency. In fact, we detected increased AMPK-alpha phosphorylation levels in Akk-treated jejunal epithelial cells both in vivo and in vitro. Furthermore, activating AMPK inhibits lipids absorption in jejunum. Thus, we conclude that oral administration of Akk activates the AMPK pathway and represses the lipid absorption in jejunal epithelial cells, which contributes to the metabolic benefits of oral Akk administration.

2025-01-25 | GSE254234 | GEO

Intestinal Akkermansia muciniphila complements the therapeutic efficacy of PD1 therapy by reshaping the immunosuppressive microenvironment in nonalcoholic fatty liver disease (NAFLD)-induced hepatocellular carcinoma [16S]

Project description:16S rRNA sequencing showed that Akkermansia muciniphila (Akk) decreased during the course of HCC tumor development, and daily administration of Akk not only ameliorated liver steatosis and cholesterol biosynthesis but also effectively attenuated the development of NAFLD-induced HCC.

2024-11-29 | GSE242468 | GEO

Project description:The mechanism underlying negative regulatory role of Akk in hepatic steatosis was examined using bulk RNA sequencing.

2024-11-29 | GSE242467 | GEO

Project description:Akk&renal injury

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Intestinal Akkermansia muciniphila predicts clinical response to PD1 blockade in advanced non-small cell lung cancer patients [RNA-seq].

Project description:The endpoint of this study was to prospectively validate the prognostic significance of fecal Akk in advanced NSCLC patients treated with first or second line ICI. We performed RNA sequencing to compare transcriptomic profiles of the different groups.

2021-08-20 | GSE182328 | GEO

Inflammatory bowel disease risk loci overlap with DNA regulatory regions in immune cells and intestinal epithelium

Project description:Background & Aims: The contribution of genetics to the pathogenesis of inflammatory bowel disease (IBD) has been established by twin studies, targeted sequencing and genome-wide association studies (GWASs). This has yielded a plethora of risk loci with an aim to identify causal variants. Research on the genetic components of IBD has mainly focused on protein coding genes, thereby omitting other functional elements in the human genome i.e. the regulatory regions. Methods: Using acetylated histone 3 lysine 27 (H3K27ac) chromatin immunoprecipitation and sequencing (ChIP-seq), we identified tens of thousands of potential regulatory regions that are active in intestinal epithelium and immune cells, the main cell types involved in IBD. We correlated these regions with susceptibility loci for IBD. Results: We show that 45 out of 163 single nucleotide polymorphisms (SNPs) associated with IBD co-localize with active regulatory elements. In addition, another 47 IBD associated SNPs co-localize with active regulatory element via other SNP in strong linkage disequilibrium. Altogether 92 out of 163 IBD-associated SNPs can be connected with distinct regulatory element. This is 2.5 to 3.5 times more frequent than expected from random sampling. The genomic variation in these SNPs often creates or disrupts known binding motifs - thereby possibly affecting the binding affinity of transcriptional regulators and altering the expression of regulated genes. Conclusions: We show that in addition to protein coding genes, non-coding DNA regulatory regions, active in immune cells and in intestinal epithelium, are involved in IBD. H3K27ac ChIP-seq (ab4729, Abcam) profile of 7 intestinal epithelial samples

2013-12-06 | E-GEOD-51425 | biostudies-arrayexpress

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