GNPS Mono-Colonized GF Reporter Mice
Ontology highlight
ABSTRACT:
INSTRUMENT(S): Q Exactive
ORGANISM(S): Mus Musculus (ncbitaxon:10090)
SUBMITTER: 
Pieter C Dorrestein
PROVIDER: MSV000088040 | GNPS | Tue Aug 31 20:43:00 BST 2021
REPOSITORIES: GNPS
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Project description:Mono-colonized GF reporter mice fecal metabolomics by LC-MS/MS
2021-08-31 | MSV000088040 | MassIVE
Project description:Purpose: Gut microbiota-derived metabolites play a pivotal role in the maintenance of local gut homeostasis and can even induce systemic effects via accumulation in the bloodstream. Here, we demonstrate that mono-colonization of germ-free (GF) mice with Clostridium sporogenes protects mice from inflamation and death induced by DSS colitis. Method: 8-12-week-old male mice (GF, SPF and GF colonized with C. sporogenes (CS)) were treated with 2.5% DSS in drinking water for 5 days and colon tissue was isolated on day 7. RNA was isolated from the colon tissue and RNA sequenzing was performed. Results: Mono-colonization of GF mice with Clostridium sporogenes protected the mice from DSS colitis induced death, while producing high amounts of indole-3-propionic acid (IPA), branched chain (BCFA) and short-chain (SCFA) fatty acids. In comparison to CS mice, SPF mice showed much higher levels of inflammatory related genes and a worse histological score. Conclusion: Histological stainings and the RNAseq both showed high levels of protection of C. sporogenes colonized mice in colitis, compared to SPF and GF animals. The data provide evidence for a therapeutic potential of C. sporogenes for IBD patients.
2024-10-15 | GSE264024 | GEO
Project description:Lactobacillus NK2 (L.NK2) is a commensal microbe, isolated from the mouse intestinal feces in our lab. To examine the potential role of L. NK2 in the gut immunity, we monocolonized GF mice with L.NK2. And, we conducted a microarray experiment to compare the transcriptomes of GF and L.NK2-colonized mice intestines under the same experimental condition We used microarrays to detail the global programme of gene expression in intestinal epithelial cells (IEC) and Peyer's patches cells (PP) of GF and L.NK2-colonized mice.
2018-03-01 | GSE111111 | GEO
Project description:While microbiome and pregnancy are known to alter drug disposition, the interplay of the two physiological factors to impact expression and/or activity of drug processing genes (DPGs) has yet to be elucidated. This study aimed to investigate the effects of microbiome on host hepatic DPGs during pregnancy using conventional (CV) and germ-free (GF) mice. Four groups of female mice were used, namely CV non-pregnant (CVNP), GF non-pregnant (GFNP), CV pregnant (CVP), and GF pregnant (GFP) mice. Pregnant mice examined were on gestation day 15. Transcriptomic and targeted proteomics of hepatic DPGs were profiled using a multi-omics approach. Plasma bile acid and steroid hormone levels were quantified using LC-MS/MS. Cyp3a activities were measured by mouse liver microsome incubations. While the overall trend in pregnancy-induced changes in the expression or activity of hepatic DPGs in CV and GF mice was similar, significant differences in the magnitude of changes were observed. For certain genes, we noticed opposite effects of pregnancy on mRNA and protein expression of DPGs in both CV and GF mice. For instance, the mRNA levels of Cyp3a11, the murine homolog of human CYP3A4, were decreased by 1.7-fold and 3.3-fold by pregnancy in CV and GF mice, respectively. However, the protein levels of Cyp3a11 were increased similarly ~2-fold by pregnancy in both CV and GF mice. Yet, microsome incubations revealed a marked induction of Cyp3a activity by pregnancy that was >5-fold greater in CV mice than that in GF mice. Plasma bile acid and steroid hormone levels were also significantly altered by microbiome and pregnancy, respectively, which may contribute to the differential effects of pregnancy in CV and GF mice. This is the first study to show that microbiome can alter hepatic DPGs in pregnancy.
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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:We sequenced mRNA from 12 samples extracted from mouse amygdala tissue to generate the first amygdala-specific murine transcriptome for germ-free mice (GF), conventionally raised controls (CON) and germ-free mice that have been colonized with normal microbiota from postnatal day 21 (exGF). Equal amounts of RNA from two to three animals were pooled to yield 4 samples per group (CON, GF, and exGF). Pairwise comparisons for CONvsGF, CONvsexGF, GFvsexGF were performed using DESeq2.
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Project description:In this study, we performed LC-QTOF-MS-based metabolomics and RNA-seq based transcriptome analysis using seven tissues of M. japonicus.
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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.
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Project description:We sequenced mRNA from 12 samples extracted from mouse amygdala tissue to generate the first amygdala-specific murine transcriptome for germ-free mice (GF), conventionally raised controls (CON) and germ-free mice that have been colonized with normal microbiota from postnatal day 21 (exGF).
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