Homo sapiens strain:TIG-3 cells
Ontology highlight
ABSTRACT:
PROVIDER: PRJDB11247 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| DRR280678.fastq.gz | Fastqsanger.gz | |||
| DRR280679.fastq.gz | Fastqsanger.gz | |||
| DRR280680.fastq.gz | Fastqsanger.gz | |||
| DRR280681.fastq.gz | Fastqsanger.gz | |||
| DRR280682.fastq.gz | Fastqsanger.gz |
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Project description:Beta cell dysfunction, caused by metabolic and inflammatory stress, contributes to the development of type 2 diabetes. Butyrate, produced by the gut microbiota, has shown beneficial effects on glucose metabolism and may directly affect beta cell function, but the mechanisms are poorly described. The aim of this study was to investigate the effect of butyrate on IL-1β-induced β cell dysfunction. We showed that long-term exposure of mouse islets to non-cytotoxic concentrations of IL-1β impaired insulin secretion and content and reduced proliferation. This dysfunction was prevented when the islets were exposed to butyrate and butyrate alone also boosted insulin secretion. In contrast, butyrate further downregulated the proliferation. To get a better indication of mechanisms of actions we investigated the global mRNA expression profiles using RNA sequencing. Our results indicated that the protective effects of butyrate are associated with upregulation of secretion/transport-related genes and downregulation of inflammatory genes induced by IL-1β. In addition, several cell cycle related genes were strongly inhibited by butyrate. In conclusion, butyrate plays an essential role in supporting beta cell function under inflammatory conditions, suggesting a potential for therapeutic use in treatment and prevention of T2D.
2021-09-27 | GSE180317 | GEO
Project description:Identification of gut bacteria enriched in colorectal cancer patients with the ability to promote tumorigenesis via butyrate secretion
| PRJDB11246 | ENA
Project description:The balance between tolerogenic and inflammatory responses determines immune homeostasis in the gut. Dysbiosis and a defective host defense against invading intestinal bacteria can shift this balance via bacterial-derived metabolites and trigger chronic inflammation. We show that the short chain fatty acid butyrate modulates monocyte to macrophage differentiation by promoting antimicrobial effector functions. The presence of butyrate modulates antimicrobial activity via a shift in macrophage metabolism and reduction in mTOR activity. This mechanism is furthermore dependent on the inhibitory function of butyrate on histone deacetylase 3 (HDAC3) driving transcription of a set of antimicrobial peptides including calprotectin. The increased antimicrobial activity against several bacterial species is not associated with increased production of conventional cytokines. Butyrate imprints antimicrobial activity of intestinal macrophages in vivo. Our data suggest that commensal bacteria derived butyrate stabilize gut homeostasis by promoting antimicrobial host defense pathways in monocytes that differentiate into intestinal macrophages.
2019-01-30 | GSE111049 | GEO
Project description:Pathogenic bacteria export large proteins and protein complexes, including virulence factors, using dedicated trans-envelope multi-protein machineries, collectively called secretion systems. Four of these protein export machines found in Gram-negative bacteria: type 2 and 3 secretion systems, the type 4 pilus biogenesis system and the filamentous phage assembly-secretion system (FFSS), contain large homologous gated channels in the outer membrane, called secretins. These channels are radially symmetrical homomultimers (luminal diameter 6-8 nm) interrupted by an internal septum, which blocks the channel in its resting state. By analyzing the transcriptome of Escherichia coli producing the FFSS secretin pIV and an isogenic leaky-gate variant, we have expanded the known secretin responses to include the Sox, Cpx, Rcs and RyhB regulons, in addition to the known secretin responder, the Psp regulon. Furthermore, we show that responses dependent on transcriptional regulators CpxR, SoxS and RcsB (in addition to PspF) are required for survival of E. coli producing the leaky-gate variant of secretin pIV, while CpxR, SoxS and PspF are required for survival of cells producing wild-type T3SS secretin InvG. Our analysis shows that secretins induce three out of six envelope stress responses and responses to oxidative stress. Identification of the key stress response regulators required for survival of secretin stress suggests pathways that may be of interest in developing strategies for control of secretin-expressing pathogenic bacteria.
2021-01-31 | GSE85194 | GEO
Project description:Pancreatic ductal adenocarcinoma (PDAC) is a highly aggressive disease with limited therapeutic options. The diversity and composition of intra-tumoral microbiota are associated with PDAC outcomes, and modulating the tumor microbiota has the potential to influence tumor growth and host-immune response. Here, we explore whether intervention with butyrate-producing probiotic can limit PDAC progression. By analyzing TCGA (PAAD) dataset, we found that tumoral butyrate-producing microbiota links to better prognosis and less aggressive features of PDAC. Intervention with Clostridium butyricum or its metabolite butyrate triggered superoxidative stress and intracellular lipid accumulation, which enhanced ferroptosis susceptibility of PDAC. Our study reveals a novel antitumor mechanism of butyrate, and suggests the therapeutic potential of butyrate-producing probiotics in PDAC.
2025-03-15 | GSE227418 | GEO
Project description:Recently, we established Corynebacterium glutamicum as a suitable production host for various bacteriocins including garvicin Q (GarQ). Here, we establish secretion of GarQ by C. glutamicum via the Sec translocon. At neutral pH, the cationic peptide is efficiently adsorbed to the negatively charged envelope of producer bacteria limiting availability of the bacteriocin in culture supernatants. Using a reporter strain and proteomic analyses, we identified HtrA, a protease associated with secretion stress, as another potential factor limiting GarQ production.
2024-01-08 | PXD046499 | Pride
Project description:Activation of free fatty acid receptor 2 (FFAR2) on enteroendocrine L-cells mediates secretion of glucagon-like peptide 1 (GLP-1) and peptide YY (PYY), key regulators of central appetite control with therapeutic relevance to obesity. Here, we show that butyrate, a metabolite derived from fermentation of dietary fibre and an FFAR2 agonist, stimulates a PYY-biased profile in a human L-cell model at the transcriptional, morphological and secretory level via an FFAR2-Gai axis that does not require dynamin-dependent receptor internalization. We observe that butyrate modulates active Notch cascades within a Hes1-GFP mouse organoid model, which are antagonistic to secretory differentiation, and identify butyrate-dependent regulation of late-stage human enteroendocrine maturation markers, NeuroD1 and Pax6. Butyrate-mediated upregulation of Pyy and Pax6 is enhanced by the FFAR2-selective Gai biased allosteric agonist AZ-1729. Our study reveals functions of spatiotemporally regulated butyrate-activated FFAR2 signalling mechanisms that could be pharmacologically amplified to fine-tune L-cell populations in the human colon.
2026-02-24 | GSE320030 | GEO
Project description:Background: Humans with metabolic and inflammatory diseases frequently harbor lower levels of butyrate-producing bacteria in their gut. However, it is not known whether variation in the levels of these organisms is causally linked with disease development and whether diet modifies the impact of these bacteria on health. Results: We use germ-free apolipoprotein E-deficient mice colonized with synthetic microbial communities that differ in their capacity to generate butyrate to demonstrate that Roseburia intestinalis interacts with dietary components to (i) impact gene expression in the intestine, directing metabolism away from glycolysis and toward fatty acid utilization, (ii) improve intestinal barrier function, (iii) lower systemic inflammation and (iv) ameliorate atherosclerosis. Furthermore, intestinal administration of butyrate improves gut barrier function and reduces atherosclerosis development. Conclusions: Altogether, our results illustrate how modifiable diet-by-microbiota interactions impact cardiovascular disease, and suggest that interventions aimed at increasing the representation of butyrate-producing bacteria may provide protection against atherosclerosis.
2018-08-29 | GSE119141 | GEO
Project description:Butyrate induces Treg via HDACi activity Microarray of DC treated with TSA or Butyrate over untreated
2013-10-15 | E-GEOD-51263 | biostudies-arrayexpress