Similar Datasets
Project description:To investigate SFB-host interactions and the host response to SFB, we compared gene expression profiles in terminal ileal mucosa collected from 5 SFB-positive and 5-negative age-matched patients identified from SFB PCR. We observed that 472 genes were different between the two groups (P < 0.05). Among them, 290 genes were up-regulated and 182 were down-regulated. GO biological pathway analysis of up-regulated genes revealed positive regulation of T-cell differentiation and activation pathways were enhanced (P < 0.001), suggesting that SFB colonization stimulated the human immune system, specifically T-cell maturation. Indeed, enhanced expression of Cd3e, Ifng, IL10, Foxp3 was observed in terminal ileal mucosa of 5 SFB-positive patients.
2015-05-01 | GSE68425 | GEO
Project description:To investigate SFB-host interactions and the host response to SFB, we compared gene expression profiles in terminal ileal mucosa collected from 5 SFB-positive and 5-negative age-matched patients identified from SFB PCR. We observed that 472 genes were different between the two groups (P < 0.05). Among them, 290 genes were up-regulated and 182 were down-regulated. GO biological pathway analysis of up-regulated genes revealed positive regulation of T-cell differentiation and activation pathways were enhanced (P < 0.001), suggesting that SFB colonization stimulated the human immune system, specifically T-cell maturation. Indeed, enhanced expression of Cd3e, Ifng, IL10, Foxp3 was observed in terminal ileal mucosa of 5 SFB-positive patients. To find immune-related genes significantly expressed (p < 0.05) between SFB-positive and -negative
2015-05-01 | E-GEOD-68425 | biostudies-arrayexpress
Project description:H3K27Ac enrichment in intestinal epithelial cells from intestine of germ-free and segmented filamentous bacteria (SFB)-monoassociated mice. Intestinal epithelial cells were harvested from the terminal ileum of germ-free or SFB mice. Chromatin immunoprecipitation was performed with anti-H3K27Ac. Sequencing was performed using the Illumina HiSeq2500. Reads were mapped to the mm10 genome using Bowtie.
2022-11-08 | GSE182628 | GEO
Project description:Vertebrates typically harbor a rich gastrointestinal microbiota, which has co-evolved with the host over millennia and is essential for several of its physiological functions, in particular maturation of the immune system. Recent studies have highlighted the importance of a single bacterial species, segmented filamentous bacteria (SFB), in inducing a robust T helper (Th)17 population in the small intestinal lamina propria (SI-LP) of the mouse gut. Consequently, SFB can promote IL-17-dependent immune and autoimmune responses, gut-associated as well as systemic, including inflammatory arthritis and experimental autoimmune encephalomyelitis. Here, we exploit the incomplete penetrance of SFB colonization of NOD mice in our animal facility to explore its impact on the incidence and course of type-1 diabetes in this prototypical, spontaneous model. There was a strong co-segregation of SFB-positivity and diabetes protection in females, but not in males, which remained relatively disease-free regardless of the SFB status. In contrast, insulitis did not depend on SFB colonization. SFB-positive, but not SFB-negative, females had a substantial population of Th17 cells in the SI-LP, which was the only significant, repeatable difference in the examined T cell compartments of the gut, pancreas or systemic lymphoid tissues. Th17 signature transcripts dominated the very limited SFB-induced molecular changes detected in SI-LP CD4+ T cells. Thus, a single bacterium, and the gut immune system alterations associated with it, can either promote or protect from autoimmunity in predisposed mouse models, likely reflecting their variable dependence on different Th subsets.
2011-06-09 | GSE29806 | GEO
Project description:Purpose: The goals of this study are to compare RNAs bound by translating ribosomes in the presence or absence of Segmented Filamentous Bacteria (SFB) colonization of the small intestine Methods: EDTA fractions containing small intestine epithelial cells from SFB negative and SFB positive mice were harvested. TRAP assay enriching for ribosome bound fraction were enriched using anti-GFP antibodies against GFP-ribosomeL10 fusion protein. mRNA profiles were generated by deep sequencing, using Illumina HighSeq. The sequence reads that passed quality filters were analyzed at the transcript isoform level with two methods: Burrows–Wheeler Aligner (BWA) and TopHat followed by CuffDiff. qRT–PCR validation was performed using SYBR Green assays. Results: SFB colonization upregulate a subset of mRNAs being translated by ribosomes. Conclusions: SFB changes small intestine epithelial cell translation profile.
2015-10-09 | GSE70598 | GEO
Project description:Hepatocellular carcinoma (HCC) is the fourth most frequent cause of cancer-related mortality worldwide. While ablation, resection and orthotopic liver transplantation are indicated at an early stage of the disease, Sorafenib (Sfb) is the current most administrated first-line treatment for advanced HCC, even thought its therapeutic benefit is limited as a consequence of the appearance of resistances. Deep knowledge on the molecular consequences of Sfb-treatment is essentially required for optimizing novel therapeutic strategies to improve the outcomes for patients with advanced HCC. In this study, we analysed differential gene expression changes in two well characterized HCC cell lines upon a Sfb-treatment, demonstrating that both lines responded similarly to the treatment. Our results provide valuable information on the molecular action of Sfb on diverse cellular fundamental processes such as DNA repair, translation and proteostasis and identify rationalization issues that could give a different therapeutic perspective to Sfb.
2022-02-24 | GSE186280 | 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:Vertebrates typically harbor a rich gastrointestinal microbiota, which has co-evolved with the host over millennia and is essential for several of its physiological functions, in particular maturation of the immune system. Recent studies have highlighted the importance of a single bacterial species, segmented filamentous bacteria (SFB), in inducing a robust T helper (Th)17 population in the small intestinal lamina propria (SI-LP) of the mouse gut. Consequently, SFB can promote IL-17-dependent immune and autoimmune responses, gut-associated as well as systemic, including inflammatory arthritis and experimental autoimmune encephalomyelitis. Here, we exploit the incomplete penetrance of SFB colonization of NOD mice in our animal facility to explore its impact on the incidence and course of type-1 diabetes in this prototypical, spontaneous model. There was a strong co-segregation of SFB-positivity and diabetes protection in females, but not in males, which remained relatively disease-free regardless of the SFB status. In contrast, insulitis did not depend on SFB colonization. SFB-positive, but not SFB-negative, females had a substantial population of Th17 cells in the SI-LP, which was the only significant, repeatable difference in the examined T cell compartments of the gut, pancreas or systemic lymphoid tissues. Th17 signature transcripts dominated the very limited SFB-induced molecular changes detected in SI-LP CD4+ T cells. Thus, a single bacterium, and the gut immune system alterations associated with it, can either promote or protect from autoimmunity in predisposed mouse models, likely reflecting their variable dependence on different Th subsets. All gene expression profiles were obtained from highly purified T cell populations sorted by flow cytometry. Cells were sorted from individual mice with at least four replicates generated for all groups. RNA from 1-5 x 104 cells was amplified, labeled, and hybridized to Affymetrix Mo GENE 1.0ST microarrays. Raw data were preprocessed with the RMA algorithm in GenePattern, and averaged expression values were used for analysis.
2011-06-09 | E-GEOD-29806 | biostudies-arrayexpress
Project description:We have performed ChIP-sequencing analysis on human FOXN2 and RFX1 target sequences in human embryonic kidney HEK293T cells stably expressing Streptavidin-S-FLAG (SFB) triple-tagged proteins. The NGS sequencing were performed on Illumina MiSeq desktop sequencer.
2015-01-01 | E-MTAB-3120 | biostudies-arrayexpress
Project description:Commensal bacteria influence host physiology, including immune responses, without invading host tissues. We show that proteins from segmented filamentous bacteria (SFB), which are immunomodulatory commensal microbes, are transferred into intestinal epithelial cells by adhesion-directed endocytosis that is distinct from the clathrin-dependent endocytosis of invasive pathogens. SFB transfer microbial cell wall-associated proteins, including an antigen that stimulates mucosal Th17 cell differentiation, into the cytosol of epithelial cells. Removal of CDC42 activity in vivo led to disruption of endocytosis induced by SFB, decreased epithelial antigen acquisition with consequent loss of immune modulation by SFB-specific CD4 T cells and mucosal Th17 cells. Our findings indicate direct communication between a resident gut microbe and the host and show that intestinal epithelial cells acquire antigens from commensal bacteria for generation of T-cell responses to the resident microbiota.
2019-01-10 | GSE124848 | GEO