Mouse feces metabolome conventional vs germfree
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB42207 | ENA |
REPOSITORIES: ENA
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Project description:With this study we wanted to evaluate the impact of murine norovirus infection of germfree mice and to compare it to germfree mice which have received fecal transplants of conventional mice.
2014-11-13 | GSE60163 | GEO
Project description:Microarray transcriptome analysis of colonocytes from conventionally raised and germfree mice. 12 samples were analyzed, with 6 germfree (GF) samples vs. 6 conventionally raised (CONV) samples.
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Project description:To gain insight into host-microbe interactions in a piglet model, a functional genomics approach has been applied to address the working hypothesis that transcriptionally regulated genes associated with promoting epithelial barrier function evolved as a defensive response to the intestinal microbiota. Cesarean-derived germfree (GF) newborn piglets were colonized with adult swine feces, and villus and crypt epithelial cell transcriptomes from colonized and GF neonatal piglets were compared using laser-capture microdissection and high-density porcine oligonucleotide microarray technology. Consistent with our hypothesis, results revealed that resident microbiota induces the expression of genes encoding proteins involved in promoting intestinal epithelial cell turnover and mucus biosynthesis and priming of the immune system. Furthermore, differential expression of genes associated with antigen presentation (SLA-7, B2M, TAP1 and TAPBP) demonstrates that microbiota induced immune responses using a distinct regulatory mechanism common for these genes. Intestinal microbiota stimulated interferon (IFN) receptor-mediated signaling cascade using signal transducer and activator of transcription-1 (STAT1), STAT2 and IFN regulatory factor-7 transcription factors to activate IFN-inducible genes. In addition, excessive inflammatory responses were prevented by activating RNA expression of inhibitory-kappa-B and Toll-interacting protein, along with downregulating the expression of a gene encoding GATA binding protein-1 consistent with the maintenance of intestinal homeostasis. This study supports the concept that the intestinal epithelium has evolved to maintain a physiological state of inflammation with respect to continuous microbial exposure, which serves to maintain tight intestinal barrier but prevent overt inflammatory responses that would compromise barrier function. Keywords: oligonucleotide array
2008-03-04 | GSE7232 | GEO
Project description:Germfree (GF) mice have been used as a model to study the contribution of the intestinal microbiota to metabolic energy balance of the host. Despite a wealth of knowledge accumulated since the 1940’s, the response of GF mice to a high fat diet is largely unknown. In the present study, we compared the metabolic consequences of a high fat (HF) diet on GF and conventional (Conv) C57BL/6J mice. As expected, Conv mice developed obesity and glucose intolerance with a HF diet. In contrast, GF mice remained lean and resisted the HF diet-induced insulin resistance. The anti-obesity phenotype of GF/HF mice was accompanied by reduced caloric intake, diminished food efficiency, and excessive fecal lipid excretion contributed to the reduced food efficiency. In addition, HF diet-induced hypercholesterolemia was ameliorated, which was partially due to an increase in fecal cholesterol excretion. However, hepatic cholesterols were increased in GF/HF mice. Elevated nuclear SREBP2 proteins and the up-regulation of cholesterol biosynthesis genes support the increased liver cholesterol biosynthesis in GF/HF mice. The resistance to HF diet-induced metabolic abnormalities in GF mice was also associated with a reduced immune response, indicated by low plasma pro-inflammatory and anti-inflammatory markers. These data suggest that the gut microbiota of Conv mice contributes to HF diet-induced obesity, insulin resistance, dyslipidemia and hepatic steatosis in mice. Thus, results of the present study describe the metabolic responses of GF mice to a HF diet and further our understandings of the relationship between the gut microbiota and the host. Germfree and conventional C57BL/6J mice were fed with a high fat diet for 11 weeks. Then, all mice were sacrified under 10-h food deprevation, and liver samples of germfree (n=14) and conventional (n=16) were examined.
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Project description:Microarray transcriptome analysis of colonocytes from conventionally raised and germfree mice.
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Project description:Transcriptional profiling of Caco-2 cells comparing Caco-2 monolayers cultured in a custom built co-culture chamber, either inside a 5% CO₂ incubator (conventional cell culture environment) or an anaerobic workstation (apical anaerobic environment) for 12 hours. Two-condition experiment with dye swap, A vs B, 6 biological replicates
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Project description:Feces 16s rRNA seq experiments is required to demonstrate the AZ1 doesn’t impact the intestinal microbiota.
2020-02-14 | GSE143003 | GEO
Project description:The intestinal tract is inhabited by a large and diverse community of microbes collectively referred to as the gut microbiota. While the gut microbiota provides important benefits to its host, especially in metabolism and immune development, disturbance of the microbiota–host relationship is associated with numerous chronic inflammatory diseases, including inflammatory bowel disease and the group of obesity-associated diseases collectively referred to as metabolic syndrome. A primary means by which the intestine is protected from its microbiota is via multi-layered mucus structures that cover the intestinal surface, thereby allowing the vast majority of gut bacteria to be kept at a safe distance from epithelial cells that line the intestine1. Thus, agents that disrupt mucus–bacterial interactions might have the potential to promote diseases associated with gut inflammation. Consequently, it has been hypothesized that emulsifiers, detergent-like molecules that are a ubiquitous component of processed foods and that can increase bacterial translocation across epithelia in vitro2, might be promoting the increase in inflammatory bowel disease observed since the mid-twentieth century3. Here we report that, in mice, relatively low concentrations of two commonly used emulsifiers, namely carboxymethylcellulose and polysorbate-80, induced low-grade inflammation and obesity/metabolic syndrome in wild-type hosts and promoted robust colitis in mice predisposed to this disorder. Emulsifier-induced metabolic syndrome was associated with microbiota encroachment, altered species composition and increased pro-inflammatory potential. Use of germ-free mice and faecal transplants indicated that such changes in microbiota were necessary and sufficient for both low-grade inflammation and metabolic syndrome. These results support the emerging concept that perturbed host–microbiota interactions resulting in low-grade inflammation can promote adiposity and its associated metabolic effects. Moreover, they suggest that the broad use of emulsifying agents might be contributing to an increased societal incidence of obesity/metabolic syndrome and other chronic inflammatory diseases.
In Study Design factor “Treatment” CMC stands for carboxymethylcellulose and P80 for polysorbate-80
Research is published:
http://www.nature.com/nature/journal/v519/n7541/full/nature14232.html
2015-06-11 | ST000203 | MetabolomicsWorkbench