Mus musculus
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ABSTRACT:
PROVIDER: PRJNA355113 | ENA |
REPOSITORIES: ENA
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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).
2017-11-25 | GSE90577 | GEO
Project description:We report that adhesion of microbes to intestinal epithelial cells is a critical cue for Th17 induction. SFB colonized in the intestine of mice can adhere to mouse small intestinal epithelial cells and induce intestinal Th17 cells. However, SFB colonized in rats cannot adhere to mouse intestinal epithelial cells and induce Th17 cells. Likewise, Citrobacter rodentium (WT) can adhere to mouse colonic epithelial cells and induce Th17 cells, but non-adherent mutant of C. rodentium (Δeae) cannot induce Th17 cells. To examine the influence of adherent bacteria on intestinal epithelial cells, we performed RNA seq. Germ free mice were orally inoculated with M-SFB or R-SFB and total RNA was isolated from small intestinal epithelial cells 1 week after inoculation. Alternatively, germ free mice were orally inoculated with C. rodentium WT or eae mutant and total RNA was isolated from colonic epithelial cells 5 days after inoculation. The gene expression of small intestinal epithelial cells isolated from small intestine of germ free mice (2 mice), mice monocolonized with M-SFB (2 mice) or R-SFB (3 mice), and colon of germ free mice (3 mice), mice monocolonized C. rodentium WT (3 mice) or eae mutant (3 mice).
2015-09-24 | E-GEOD-71734 | biostudies-arrayexpress
Project description:We report that adhesion of microbes to intestinal epithelial cells is a critical cue for Th17 induction. SFB colonized in the intestine of mice can adhere to mouse small intestinal epithelial cells and induce intestinal Th17 cells. However, SFB colonized in rats cannot adhere to mouse intestinal epithelial cells and induce Th17 cells. Likewise, Citrobacter rodentium (WT) can adhere to mouse colonic epithelial cells and induce Th17 cells, but non-adherent mutant of C. rodentium (Δeae) cannot induce Th17 cells. To examine the influence of adherent bacteria on intestinal epithelial cells, we performed RNA seq. Germ free mice were orally inoculated with M-SFB or R-SFB and total RNA was isolated from small intestinal epithelial cells 1 week after inoculation. Alternatively, germ free mice were orally inoculated with C. rodentium WT or eae mutant and total RNA was isolated from colonic epithelial cells 5 days after inoculation.
2015-09-24 | GSE71734 | GEO
Project description:Expression in intestinal epithelial cells from intestine of germ-free and segmented filamentous bacteria (SFB)-monoassociated mice during infection. Intestinal epithelial cells were harvested from the terminal ileum of germ-free or SFB mice infected with Citrobacter rodentium for 6 days. RNA was isolated using RNeasy Kit (Qiagen). Sequencing was performed using the Illumina HiSeq2500. Reads were mapped to the mm10 genome using Bowtie.
2022-11-08 | GSE182630 | GEO
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 mediates colitis recovery via interleukin 22 pathway activation and Card9-/- mice have enhanced susceptibility to colitis. To reveal the mechanisms responsible of this defect in Card9-/-mice, we compared colon transcriptomics in WT and Card9-/- mice before and during DSS-induced colitis. Mice transcriptomes clusterized according to the genotype supporting a pattern clearly different in WT and Card9-/- mice. The number of up-regulated genes at day 7 was largely higher in Card9-/- compared to WT mice. Pathway analyses of the induced transcripts showed a dominance of immune-related pathway with a stronger signal in Card9-/- mice. Interestingly, NOD-like receptor signaling pathway, in which CARD9 is involved, was an exception with weaker activation in Card9-/- than in WT mice. During the recovery period at day 12, pathways involved in cell proliferation and replication were significantly activated in WT compared to Card9-/- mice confirming the healing defect in Card9-/- mice. For the induction of colitis, mice were given drinking water supplemented with 2% (w/v) Dextran sulphate sodium (DSS) for 7 days, then allowed to recover by drinking water alone for 5 additional days. 3 mice of each groups (WT and Card9-/-) were sacrified before DSS administration. 5 WT mice and 4 Card9-/- mice were sacrified 7 days after DSS administration and 5 mice of each group were sacrified at day 12.
2016-04-05 | E-GEOD-67577 | biostudies-arrayexpress
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 mediates colitis recovery via interleukin 22 pathway activation and Card9-/- mice have enhanced susceptibility to colitis. To reveal the mechanisms responsible of this defect in Card9-/-mice, we compared colon transcriptomics in WT and Card9-/- mice before and during DSS-induced colitis. Mice transcriptomes clusterized according to the genotype supporting a pattern clearly different in WT and Card9-/- mice. The number of up-regulated genes at day 7 was largely higher in Card9-/- compared to WT mice. Pathway analyses of the induced transcripts showed a dominance of immune-related pathway with a stronger signal in Card9-/- mice. Interestingly, NOD-like receptor signaling pathway, in which CARD9 is involved, was an exception with weaker activation in Card9-/- than in WT mice. During the recovery period at day 12, pathways involved in cell proliferation and replication were significantly activated in WT compared to Card9-/- mice confirming the healing defect in Card9-/- mice. Results published in Nature Medicine, doi:10.1038/nm.4102
2016-04-05 | GSE67577 | GEO
Project description:Transcriptional profiling of intestinal response to Citrobacter rodentium in wild-type and Nlrp12-deficient mice Four-conditions experiment, Nlrp12-deficient mouse infected by Citrobacter rodentium at day 7 versus non-infected Nlrp12-deficient mice with two biologicals replicates , Wild-type mouse infected by Citrobacter rodentium at day 7 versus non-infected Wild-type mice with two biologicals replicates and Nlrp12-deficient mouse infected by Citrobacter rodentium versus Control mouse infected by Citrobacter rodentium at 2 differents times ( day 0 and post infection at day 7 ) with three biologicals replicates
2015-07-25 | E-GEOD-59940 | biostudies-arrayexpress
Project description:Germ-free (GF) mice can be used as a powerful tool to investigate the role of the intestinal commensal flora in metabolism and immune tolerance. In this study we have used whole genome transcriptome analyses to compare expression levels systemically in liver of germ-free mice and specific pathogen free (SPF) mice. Keywords: Mouse liver tissue germ-free or specific pathogen free vs universal mouse reference Specific Pathogens Excluded from the SPF mice: Virus 1. Mouse Hepatitis Virus (MHV) 2. Mouse Rotavirus (EDIM) 3. Parvoviruses Minute virus of mice (MVM) Mouse parvo virus (MPV) 4. Pneumonia virus of mice (PVM) 5. Sendai virus 6. Theiler's encephalomyelitis virus 7. Ectromelia virus 8. Lymphocytic choriomeningitis virus (LCMV) 9. Mouse adenovirus 10. Mouse cytomegalovirus 11. Reovirus type 3 Bacteria 1. Citrobacter rodentium 2. Clostridium piliforme (Tyzzer’s disease) 3. Corynebacterium kutscheri 4. Mycoplasma pulmonis 5. Pasteurellaceae 6. Salmonella spp. 7. Streptococci-β-haemolytic 8. Streptococcus pneumoniae 9. Helicobacter spp. 10. Streptobacillus moniliformis Parasite 1. Ectoparasites 2. Endoparasites
2009-09-22 | GSE14689 | GEO
Project description:We generated conditional knockout of MHCII in intestinal epithelial cells in C57BL/6 mice (I-AbΔIEC) and compared their colonic transcriptome in control and Citrobacter rodentium infected mice. I-AbWT or I-AbΔIEC mice were orally gavaged with Citrobacter rodentium DBS100
2020-02-08 | GSE144952 | GEO
Project description:Despite accepted health benefits of dietary fiber, little is known about the mechanisms by which fiber deprivation impacts the gut microbiota and alters disease risk. Using a gnotobiotic model, in which mice were colonized with a synthetic human gut microbiota, we elucidated the functional interactions between dietary fiber, the gut microbiota and the colonic mucus barrier, which serves as a primary defence against pathogens. We show that during chronic or intermittent dietary fiber deficiency, the gut microbiota resorts to host-secreted mucus glycoproteins as a nutrient source, leading to erosion of the colonic mucus barrier. Dietary fiber deprivation promoted greater epithelial access and lethal colitis by the mucosal pathogen, Citrobacter rodentium, but only in the presence of a fiber-deprived microbiota that is pushed to degrade the mucus layer. Our work reveals intricate pathways linking diet, gut microbiome and intestinal barrier dysfunction, which could be exploited to improve health using dietary therapeutics. Germ-free mice (Swiss Webster) were colonized with synthetic human gut microbiota comprising of 14 species belonging to five different phyla (names of bacterial species: Bacteroides thetaiotaomicron, Bacteroides ovatus, Bacteroides caccae, Bacteroides uniformis, Barnesiella intestinihominis, Eubacterium rectale, Marvinbryantia formatexigens, Collinsella aerofaciens, Escherichia coli HS, Clostridium symbiosum, Desulfovibrio piger, Akkermansia muciniphila, Faecalibacterium prausnitzii and Roseburia intestinalis). These mice were fed either a fiber-rich diet or a fiber-free diet for about 6 weeks. The mice were then sacrificed and their cecal tissues were immediately flash frozen for RNA extraction. The extracted RNA was subjected to microarray analysis based on Mouse Gene ST 2.1 strips using the Affy Plus kit. Expression values for each gene were calculated using robust multi-array average (RMA) method.
2016-11-21 | GSE79067 | GEO