Project description:Epithelial cells in the intestinal mucosa maintain gut homeostasis by interacting with different types of microbiota. Proper appropriate immune responses in the intestinal epithelium are essential for the preservation of the intestinal homeostasis. In the present study, we aimed to identify genotypic and phenotypic changes in mice following oral feeding of various substances which has been shown to differentially affect intestinal homeostasis. We orally fed C57BL/6 mice for either one or seven days with one of the four substances: dextran sulfate sodium (DSS); Typhoid VI Polysaccharide vaccine (Vi vaccine); antibiotic cocktails (AB) of ampicillin, vancomycin, neomycin, and metronidazole; or(probiotics)consisting of Lactobacillus Rhamnosus R0011and L. Acidophilus R0052.While DSS and AB feeding resulted in severe gut pathology characterized by infiltration of inflammatory cells, epithelium shedding, and distortion of paneth cells. Vi vaccine and probiotics feeding resulted in phenotypic improvement of the gut health characterized by epithelial cell proliferation and increased formation of tight junctions between epithelial cells. Interestingly, microarray data showed significant increase in the expression levels of genes regulating cell proliferation and intestinal homeostasis in the gut epithelium of probiotics-and Vi vaccine-fed mice compared to DSS-or AB-fed mice. In addition, expression levels of genes regulating cell death and inflammation were significantly increased in the gut epithelium of DSS- and AB-fed mice. These results suggest that intestinal homeostasis play a pivotal role in maintaining gut health and, subsequently, in protecting host against enteric bacteria and external pathogens infection.
Project description:There are 10 mice in the experiment, named REC. The mice were fed with high salt diets (5% NaCl) for 4 weeks and then fed with normal salt diets for 4 weeks. Then extracted DNA from mice gastric flora to detect changes in the gastric flora of mice.
Project description:Gemcitabine treatment shifts the intestinal microbiota of PC mice towards an inflammatory profile which may worsen mucositis and side effects observed upon chemotherapy. We explored the effect of a specific probiotics blend administered, with or without gemcitabine treatment, to PC xenografted mice.
Project description:Interventions: Colorectal cancer control group:no;Colorectal cancer probiotics group:No
Primary outcome(s): Intestinal flora metabolomics;Intestinal mucosal barrier;Inflammatory factors;Observation of clinical efficacy indicators;Intestinal flora
Study Design: Parallel
| 2759602 | ecrin-mdr-crc
Project description:Changes in intestinal flora in two model mice
Project description:By combining directed evolution and synthetic biology, we engineered novel synthetic yeasts probiotics for the dynamic modulation of intestinal inflammation. In this experiment we treated TNBS-colitis induced mice with these probiotics and test the amelioration of immune response in the transcriptional level in the colon.
Project description:Candida albicans is an opportunistic fungus that can threaten life especially in patients with candidemia. The morbidity and mortality of candidemia originating from a central venous catheter (CVC) and illicit intravenous drug use (IVDU) are increasing. However, the mechanism underlying the bloodborne C. albicans infection remains unclear. Herein, we evaluated the gut microbiome, metabolites and intestinal mucosa by constructing the mouse models with candidemia. Model mice were injected with C. albicans via tail vein. Control mice underwent sham procedures. We observed basic life characteristics, intestinal damage-related alterations using hematoxylin and eosin (H&E) staining, intestinal tight junction protein levels, and intestinal permeability in these mice. Fecal samples were analyzed by performing 16S rRNA gene sequencing of the microbiota and LC-MS metabolomics to reveal the perturbations in intestinal flora and metabolism exacerbating intestinal damage. Weight loss, a decreased survival rate, C. albicans infection spread, and colonic epithelial damage occurred in the model group. Furthermore, the intestinal flora abundance was reduced. Several probiotics, such as Lactobacillus, and butyrate-producing bacteria, including Roseburia, Lachnospiraceae, and Clostridia, were depleted, and some pathogenic bacteria, such as Escherichia-Shigella and Proteus, belonging to the Proteobacteria phylum, and the inflammation mediators Ruminococcus and Parabacteroides were enriched in model mice. Multiple differentially altered metabolic pathways were observed and mainly related to bile acid, arachidonic acid, bile secretion, and arachidonic acid metabolism. This study illustrated the effects of a bloodborne C. albicans on the intestinal microbiota, metabolites, and intestinal barrier, which may provide new insights into tests or treatments for candidemia originating from CVC or IVDU.