(1-3)-beta-D glucan Antibody
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1018703 | ENA |
REPOSITORIES: ENA
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Project description:beta-glucan induced glycolysis in HIF-1 depedent manner. We reported that beta-glucan injection in mice led to upregulated glycolysis. HIF-1a plays a major role in this process. Mice receives beta-glucan via ip for 4 days. Splenocytes were isolated for RNA sequencing.
2014-09-26 | E-GEOD-57206 | biostudies-arrayexpress
Project description:We found that beta-glucan treatment induces early induction of transcripts associated with inflammation and metabolism. Several days after beta-glucan treatment, genes associated with differentation and housekeeping remain upregulated. LPS treatment induces a strong inflammatory response. Beta-glucan did not significantly alter the macrophage response to LPS.
2021-10-01 | GSE174141 | GEO
Project description:beta-glucan induced glycolysis in HIF-1 depedent manner. We reported that beta-glucan injection in mice led to upregulated glycolysis. HIF-1a plays a major role in this process.
2014-09-26 | GSE57206 | GEO
Project description:We established a bacteria infective intestinal inflammation in turbot (Scophthalmus maximus). And found that β-glucan could significantly alleviate the phenotype of turbot intestinal inflammation. We performed single cell transcriptome analysis to study bacteria infective intestinal inflammation and the effects of β-glucan. Furthermore, we revealed that β-glucan through activates Th17 cells to alleviate intestinal inflammation in turbot.
2023-12-31 | GSE238068 | GEO
Project description:Objective: Transcriptional profiling of murine HSPC in response to β-glucan-induced innate immune training
2018-02-01 | GSE95617 | GEO
Project description:Effect of beta glucan on the intestinal microflora of rainbow trout
| PRJEB54041 | ENA
Project description:Background & Aims: Non-alcoholic fatty liver disease (NALFLD)-associated changes in gut microbiota are important drivers of disease progression toward fibrosis. Therefore, reversing microbiota alterations could ameliorate NAFLD progression. Oat beta-glucan, a non-digestible polysaccharides, has shown promising therapeutic effects on hyperlipidemia associated with NAFLD, but its impact on gut microbiota and most importantly NAFLD fibrosis remains unknown. Methods: We performed detailed metabolic phenotyping including body composition, glucose tolerance, and lipid metabolism as well as comprehensive characterization of the gut-liver axis in a western-style diet (WSD)-induced model of NAFLD and assessed the effect of a beta-glucan intervention on early and advanced liver disease. Gut microbiota was modulated using broad-spectrum antibiotic (Abx) treatment. Results: Oat beta-glucan supplementation did not affect WSD-induced body weight gain, glucose intolerance, and the metabolic phenotype remained largely unaffected. Interestingly, oat beta-glucan dampened NAFLD inflammation, associated with significantly reduced monocyte-derived macrophages (MoMFs) infiltration, fibroinflammatory gene expression, and strongly reduced fibrosis development. Mechanistically, this protective effect was not mediated by changes in bile acid composition or signaling, but was dependent on gut microbiota and was lost upon Abx treatment. Specifically, oat beta-glucan partially reversed unfavorable changes in gut microbiota, resulting in an expansion of protective taxa, including Ruminococcus, and Lactobacillus followed by reduced translocation of TLR ligands. Conclusions: Our findings identify oat beta-glucan as a highly efficacious food supplement that dampens inflammation and fibrosis development in diet-induced NAFLD. These results, along with its favorable dietary profile, suggest that it may be a cost-effective and well-tolerated approach to preventing NAFLD progression and should be assessed in clinical studies.
2024-01-01 | GSE246738 | GEO
Project description:A clone encoding carboxymethylcellulase activity was isolated during functional screening of a human gut metagenomic library using Lactococcus lactis MG1363 as heterologous host. The insert sequence revealed a glycoside hydrolase family 9 (GH9) catalytic domain with sequence similarity to a gene from Coprococcus sp. ART55/1, which is closely related to Coprocococcus eutactus. Surveys of available genomes indicated a limited distribution of GH9 domains among dominant human colonic anaerobes. Genomes of two Coprococcus-related strains showed the presence of two GH9-encoding and four GH5-encoding genes, however, the strains did not appear to be able to degrade cellulose. Instead, they grew well on beta-glucans and one of the strains also showed growth on galactomannan, galactan and glucomannan. Gene expression and proteomic analysis of Coprococcus sp. ART55/1 grown on cellobiose, beta-glucan and lichenan led to a similar change in expression in comparison to glucose. On beta-glucan and lichenan only, one of the four GH5 genes was strongly upregulated. Growth on glucomannan lead to a transcriptional response of many genes, in particular a strong upregulation of glycoside hydrolases involved in mannan degradation. Thus, beta-glucans are a major growth substrate for species related to Coprococcus eutactus, with glucomannan and galactans alternative substrates for some strains.
2020-03-10 | PXD014174 | Pride
Project description:Description of cellular and molecular landscape of vitreal immune cells following optic nerve crush injury plus intra-ocular injection of particulate β-glucan after 3days, in WT and Itgam-/- mice
2024-07-03 | GSE244627 | GEO