Project description:To increase our knowledge of the effects of Fructo oligosaccharides (FOS) on the intestinal barrier function in rats, a controlled rat infection study was performed. Two groups of rats (n=12 per group) were adapted to a diet with or without FOS. mRNA was collected from the mucosa of the cecum and changes in gene expression were assessed using an agilent rat whole genome microarray (G4131A Agilent Technologies). Results indicate that dietary FOS influences immune response and wound healing mechanisms, which will most likely affect the intestinal barrier. Keywords: Dietary treatment, cecum mucosa, Rat
Project description:To increase our knowledge of the effects of Fructo oligosaccharides (FOS) on the intestinal barrier function in rats, a controlled rat infection study was performed. Two groups of rats (n=12 per group) were adapted to a diet with or without FOS. mRNA was collected from the mucosa of the cecum and changes in gene expression were assessed using an agilent rat whole genome microarray (G4131A Agilent Technologies). Results indicate that dietary FOS influences immune response and wound healing mechanisms, which will most likely affect the intestinal barrier. Experiment Overall Design: In the present study, large-scale gene expression analysis was performed to reveal mechanistic details of FOS induced gene expression in vivo in the cecum mucosa. Wistar rats were adapted to diets with (n=12) or without FOS (n=12) for 14 days. RNA was isolated from cecum mucosal scrapings, two RNA samples from the control group were ecluded based on poor quality of RNA. Agilent rat whole genome microarray containing 44290 60-mer spots, were used to study FOS induced gene expression changes in order to better understand the FOS induced effects on the intestinal barrier of rats.
Project description:We report the side-effects of High fat diet on the cecum, and foud that the AOS10-FMT could rescure the side-effect of High fat diet in many factors
Project description:To profile the expression of circulating microRNAs (miRNAs) of mice in experimental sepsis by cecal ligation and puncture (CLP), the whole blood samples were obtained from C57BL/6 mice at 4, 8, and 24 h following CLP for miRNA expression analysis using a miRNA array (The Mouse & Rat miRNA OneArray® v3). Briefly, mice were anesthetized with a combination of ketamine and xylazine as the anesthetic/analgesic agents and a midline abdominal incision was made. The cecum was mobilized, ligated in the middle of cecum below the ileocecal valve, punctured once with a 21 G needle, and a little stool was squeeze out of the cecum to induce polymicrobial peritonitis. The abdominal wall was closed in two layers. Sham-operated mice underwent the same procedure, including opening the peritoneum and exposing the bowel, but without ligation and needle perforation of the cecum.
Project description:We reported the side-effects of High fat diet & STZ on the cecum, and found that the AOS10-FMT could rescure the side-effect of High fat diet & STZ in many factors
Project description:The large-scale application of genomic and metagenomic sequencing technologies has yielded a number of insights about the metabolic potential of symbiotic human gut microbes. Bacteria that colonize the mucosal layer that overlies the gut epithelium have access to highly-sulfated polysaccharides (i.e., mucin oligosaccharides and glycosaminoglycans), which they could potentially forage as nutrient sources. To be active, sulfatases must undergo a critical post-translational modification catalyzed in anaerobic bacteria by the AdoMet enzyme anSME (anaerobic Sulfatase-Maturating Enzyme). In the present study, we have tested the role of this pathway in the prominent gut symbiont Bacteroides thetaiotaomicron, which possesses more predicted sulfatases (28) than in the human genome and a single predicted anSME. In vitro studies revealed that deletion of its anSME (BT0238) results in loss of sulfatase activity and impaired ability to use sulfated polysaccharides as carbon sources. Co-colonization of germ-free animals with both isogenic strains, or invasion experiments involving the introduction of one then the other strain, established that anSME activity and the sulfatases that are activated via this pathway, are important fitness factors for B. thetaiotaomicron, especially when mice are fed a simple sugar diet that requires this saccharolytic bacterium to adaptively forage on host glycans as nutrients. Whole genome transcriptional profiling of wild-type and the anSME mutant in vivo revealed that loss of this enzyme alters expression of genes involved in mucin utilization and that this disrupted ability to access mucosal glycans likely underlies the observed dramatic colonization defect. Comparative genomic analysis reveals that 100% of 46 fully sequenced human gut Bacteroidetes contain homologs of BT0238 and genes encoding sulfatases, suggesting that this is an important and evolutionarily conserved feature. Three replicate samples from 4 different biological treatment groups: 1. Wild-type B. thetaiotaomicron from the cecum of gnotobiotic mice fed a simple-sugar diet; 2. chuR mutant B. thetaiotaomicron from the cecum of gnotobiotic mice fed a simple-sugar diet; 3. Wild-type B. thetaiotaomicron from the cecum of gnotobiotic mice fed a plant-rich diet; 4. chuR mutant B. thetaiotaomicron from the cecum of gnotobiotic mice fed a plant-rich diet.