Ontology highlight
ABSTRACT:
PROVIDER: PRJNA690735 | ENA |
REPOSITORIES: ENA
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Project description:Chronic inflammation is one of the major players in the obesity related metabolic syndrome. However the various inflammatory mediators appear to promote insulin resistance directly or indirectly through their ability to induce the inflammatory cascade. Interleukin-15 (IL-15) is a pro-inflammatory cytokine that is involved in the pathogenesis of different autoimmune diseases such as rheumatoid arthritis, inflammatory bowel disease and type 1 diabetes. We postulated that as a pro-inflammatory cytokine, IL-15 promotes obesity during fat excess by promoting insulin resistance from tissues involved in energy metabolism. We used microarrays to characterize the gene expression profile of the brown adipose tissue of IL-15 mice under normal diet or diet enriched with the beta3-adrenergic agonist CL 316243 Total RNA obtained from adipose tissue of wt- or IL15-KO mice under normal diet or diet enriched with the beta3-adrenergic agonist CL 316243
2014-07-01 | E-GEOD-55057 | biostudies-arrayexpress
Project description:By fermenting dietary fiber, the gut microbiota supplies carbon to host epithelial cells in the form of short-chain fatty acids and other metabolic byproducts. To track the transfer of carbon from fiber to host tissues via the microbiota and more clearly define the molecules mediating this transfer, we conducted stable isotope tracing in mice with U-13C-labeled inulin followed by untargeted metabolomics by LC-MS. Additionally, we applied this labeling approach to mice with chemically induced colitis to examine how inflammation impacts carbon transfer from the microbiota to host tissues, which may aid in understanding the development of inflammatory bowel diseases.
2021-07-04 | MSV000087752 | MassIVE
Project description:Altered Tongue Coating Microbiota in Inflammatory Bowel Diseases patients contributes to intestinal inflammation
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Project description:Salivary microbiome associated with inflammatory bowel diseases
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Project description:Imbalance in beneficial and harmful bacteria underlies gastrointestinal diseases, such as inflammatory bowel disease. Here, we demonstrated that certain E. coli strains, specifically adherent-invasive E. coli (AIEC), utilize a serine metabolism pathway to outcompete other E. coli strains in the inflamed gut. In contrast, amino acid metabolism has a minimal effect on their competitive fitness in the healthy gut. The availability of luminal serine used for the competition of E. coli is largely dependent on dietary intake, as the inflammation-induced blooms of AIEC are significantly blunted when amino acids, particularly serine, are removed from the diet. Thus, intestinal inflammation regulates the intraspecific competition between Enterobacteriaceae by eliciting their metabolic reprogramming.
2019-09-06 | GSE106412 | GEO
Project description:Inflammatory Bowel Diseases are associated with marked alterations of IECs with a subsequent loss of barrier function. To identify alterations in signaling pathways in intestinal epithelium upon inflammation, we analyzed the transcriptome of IECs from patients suffering from Crohn’s disease.
2015-12-01 | GSE72780 | GEO
Project description:Chronic inflammation is one of the major players in the obesity related metabolic syndrome. However the various inflammatory mediators appear to promote insulin resistance directly or indirectly through their ability to induce the inflammatory cascade. Interleukin-15 (IL-15) is a pro-inflammatory cytokine that is involved in the pathogenesis of different autoimmune diseases such as rheumatoid arthritis, inflammatory bowel disease and type 1 diabetes. We postulated that as a pro-inflammatory cytokine, IL-15 promotes obesity during fat excess by promoting insulin resistance from tissues involved in energy metabolism. We used microarrays to characterize the gene expression profile of the brown adipose tissue of IL-15 mice under normal diet or diet enriched with the beta3-adrenergic agonist CL 316243
2014-07-01 | GSE55057 | GEO
Project description:Damage of the intestinal epithelial barrier by xenobiotics or reactive oxygen species and a dysregulated immune response are both factors involved in the pathogenesis of inflammatory bowel diseases (IBD). Curcumin and rutin are polyphenolic compounds known to have anti-oxidant and anti-inflammatory activities, but their mechanism(s) of action are yet to be fully elucidated. Mdr1a-/- mice spontaneously develop intestinal inflammation, predominantly in the colon, with pathology similar to IBD, so this mouse model is relevant for studying diet-gene interactions and potential effects of foods on remission or development of IBD. This study tested whether the addition of curcumin or rutin to the diet would alleviate colonic inflammation in mdr1a-/- mice. Using whole-genome microarrays, the effect of dietary curcumin on gene expression in colon tissue was also investigated. Twelve mice were randomly assigned to each of three diets; control (AIN-76A), control + 0.2% curcumin or control + 0.1% rutin and monitored from the age of 7 to 24 weeks. Curcumin, but not rutin, significantly reduced histological signs of colonic inflammation in mdr1a-/- mice. Microarray and pathway analyses suggested that the effect of dietary curcumin on colon inflammation could be via an up-regulation of xenobiotic metabolism and a down-regulation of pro-inflammatory pathways probably mediated by PXR and PPARï¡ activation of RXR. These results reveal the potential of global gene expression and pathway analyses to study and better understand the effect of foods in colonic inflammation. Experiment Overall Design: Twelve mice were randomly assigned to each of three diets; control (AIN-76A), control + 0â¢2% curcumin or control + 0â¢1% rutin and monitored from the age of 7 to 24 weeks. As only curcumin significantly reduced colonic HIS, comparison of the gene expression levels in colon was carried out using total RNA from colon tissue of four mdr1a-/- mice from the control group (high HIS) and four mdr1a-/- mice from the curcumin group (low HIS). A reference design with eight arrays was used for this comparison, where each individual RNA sample was hybridized in the array with the reference RNA, totalizing 4 biological replicates per treatment.
2008-06-11 | E-GEOD-10684 | biostudies-arrayexpress
Project description:We hypothesized that adipocytes can be triggered by asbestos fibers to produce an inflammatory response. Microarray-based gene expression analysis was thus carried out to identify potential inflammation-related candidates with altered expression in adipocytes following asbestos exposure. We found changes in the expression of some inflammation-related genes in adipocytes treated with the different types of asbestos fibers Cultured adipocytes were treated with 3 different types of asbestos fibers: chrysotile, crocidolite and amosite fibers at 10 mg/cm2 for 72 hours. Physiological saline was used as a control. Microarray was performed with duplicate for each sample.
2013-09-03 | E-GEOD-42330 | biostudies-arrayexpress