Project description:Analysis of transcriptional profiles in mDC sorted from apheresed PBMC and stimulated for 6 hours with cyclic glucan or LPS. The hypothesis tested is that cyclic glucan induces maturation and T cell-activation transcripts in human mDC. Total RNA extracted from mDC sorted from apheresed PBMC and activated for 6 hours with cyclic glucan or LPS.
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.
Project description:Analysis of transcriptional profiles in mDC sorted from apheresed PBMC and stimulated for 6 hours with cyclic glucan or LPS. The hypothesis tested is that cyclic glucan induces maturation and T cell-activation transcripts in human mDC.
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.
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.
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.
Project description:The fermentation of Zymomonas mobilis 2032 was conducted in 6% and 9% glucan-loading AFEX-pretreated corn stover hydrolysates, as well as in 7% glucan-loading AFEX-pretreated switchgrass hydrolysate, and RNA samples were collected at both glucose and xylose growth stages. Here we present a comprehensive RNA-Seq data set at both growth stages.
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.
