Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

The role of HIF-1 in beta-glucan induced response in myeloid cell

ABSTRACT: 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.

ORGANISM(S): Mus musculus

SUBMITTER: Shih-Chin Cheng

PROVIDER: E-GEOD-57206 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

mTOR- and HIF-1α-mediated aerobic glycolysis as metabolic basis for trained immunity.

Cheng Shih-Chin SC Quintin Jessica J Cramer Robert A RA Shepardson Kelly M KM Saeed Sadia S Kumar Vinod V Giamarellos-Bourboulis Evangelos J EJ Martens Joost H A JH Rao Nagesha Appukudige NA Aghajanirefah Ali A Manjeri Ganesh R GR Li Yang Y Ifrim Daniela C DC Arts Rob J W RJ van der Veer Brian M J W BM Deen Peter M T PM Logie Colin C O'Neill Luke A LA Willems Peter P van de Veerdonk Frank L FL van der Meer Jos W M JW Ng Aylwin A Joosten Leo A B LA Wijmenga Cisca C Stunnenberg Hendrik G HG Xavier Ramnik J RJ Netea Mihai G MG

Science (New York, N.Y.) 20140901 6204

Epigenetic reprogramming of myeloid cells, also known as trained immunity, confers nonspecific protection from secondary infections. Using histone modification profiles of human monocytes trained with the Candida albicans cell wall constituent β-glucan, together with a genome-wide transcriptome, we identified the induced expression of genes involved in glucose metabolism. Trained monocytes display high glucose consumption, high lactate production, and a high ratio of nicotinamide adenine dinucle ...[more]

PMID: 25258083

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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.

Dataset Information

The role of HIF-1 in beta-glucan induced response in myeloid cell

Publications

mTOR- and HIF-1α-mediated aerobic glycolysis as metabolic basis for trained immunity.

Similar Datasets

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