Project description:Laser captured cecal epithelium from gnotobiotic mice colonized with B. thetaiotaomicron or B. longum (mono-association) or B. thetaiotaomicron bi-association with B. longum. Samples were derived from 10d colonizations of NMRI mice fed a standard-chow polysaccharide rich (PR) diet. Keywords: Germ-free vs. Mono-associations or Bi-association, in vivo
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.
Project description:Laser captured cecal epithelium from gnotobiotic mice colonized with B. thetaiotaomicron or B. longum (mono-association) or B. thetaiotaomicron bi-association with B. longum. Samples were derived from 10d colonizations of NMRI mice fed a standard-chow polysaccharide rich (PR) diet. Keywords: Germ-free vs. Mono-associations or Bi-association, in vivo Total RNA was prepared from laser captured cecal epithelium of 10 day associated gnotobiotic mice, double amplified, and hybridized to 430 2.0 GeneChips or to GlycoGeneChipsv1.
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.
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.
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.
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).
Project description:We sequenced mRNA from 12 samples extracted from mouse prefrontal cortex tissue to generate the first prefrontal cortex-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).
Project description:It is crucial to decipher the host-microbiota interactions as they are involved in intestinal homeostasis and diseases. Caspase Recruitment Domain 9 (Card9) is an inflammatory bowel disease (IBD) susceptibility gene coding for an adapter protein for innate immunity toward many microorganisms. Card9-/- mice are more susceptible to colitis induced by Citrobacter rodentium as a result of impaired of the IL-22 pathway. C. rodentium is a natural mouse pathogen widely used to model human infections with Enteropathogenic Escherichia coli and Enterohaemorrhagic E. coli. To explore the role of the gut microbiota in the susceptibility of Card9-/- mice to C. rodentium infection, we colonized WT germ-free (GF) mice with the microbiota of WT (WT-->GF) or Card9-/- (Card9-/- -->GF) mice and challenged them with C. rodentium. Card9-/- -->GF mice were more susceptible than WT-->GF mice to C. rodentium. To examine the mechanisms responsible for this defect, we compared the cecum transcriptomes of WT -->GF and Card9-/- -->GF mice before and during C. rodentium-induced colitis. The number of down-regulated and up-regulated genes on day 12 after C. rodentium infection was lower in Card9-/- -->GF mice than WT-->GF mice. Card9-/- -->GF mice showed a significant down-regulation of gut morphogenesis and wound healing pathways suggesting that recovery is impaired in Card9-/- -->GF mice after C. rodentium infection. Immune response and cell division pathways were up-regulated in WT-->GF mice but not in Card9-/- -->GF confirming the defect of global response to infection when only the Card9-/- microbiota was transferred. The most induced and differentially expressed genes between Card9-/- -->GF and WT-->GF mice on day 4 after C. rodentium infection were Reg3g (encoding REGIIIγ) and Reg3b (encoding REGIIIβ).