Ontology highlight
ABSTRACT:
PROVIDER: PRJNA851244 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR19790261.fastq.gz | Fastqsanger.gz | |||
| SRR19790262.fastq.gz | Fastqsanger.gz | |||
| SRR19790263.fastq.gz | Fastqsanger.gz | |||
| SRR19790264.fastq.gz | Fastqsanger.gz | |||
| SRR19790265.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 10 |
Similar Datasets
Project description:In the presented study, in order to unravel gut microbial community multiplicity and the influence of maternal milk nutrients (i.e., IgA) on gut mucosal microbiota onset and shaping, a mouse GM (MGM) was used as newborn study model to discuss genetic background and feeding modulation on gut microbiota in term of symbiosis, dysbiosis and rebiosis maintenance during early gut microbiota onset and programming after birth. Particularly, a bottom-up shotgun metaproteomic approach, combined with a computational pipeline, has been compred with a culturomics analysis of mouse gut microbiota, obtained by MALDI-TOF mass spectrometry (MS).
2016-10-13 | PXD004033 | Pride
Project description:Background and aims. The etiopathology of inflammatory bowel diseases is still poorly understood. To date, only few little data are available on the microbiota composition in ulcerative colitis (UC), representing a major subform of inflammatory bowel diseases. Currently, one of the main challenges is to unravel the interactions between genetics and environmental factors in the onset or during the progression and maintenance of the disease. The aim of the present study was to analyse twin pairs discordant for UC for both gut microbiota dysbiosis and host expression profiles at a mucosal level and to get insight into the functional genomic crosstalk between microbiota and mucosal epithelium in vivo. Methods. Biopsies were sampled from the sigmoid colon of both healthy and diseased siblings from UC discordant twin pairs but also from healthy twins. Microbiota profiles were assessed by 16S rDNA libraries while mRNA expression profiles were analysed from the same volunteers using Affymetrix microarrays. Results. UC patients showed a dysbiotic microbiota with lower diversity and more species belonging to Actinobacteria and Proteobacteria phyla. On the contrary, their healthy siblingsM-bM-^@M-^Y microbiota contained more bacteria from the Lachnospiracea and Ruminococcaceae family than did healthy individuals . Sixty-three host transcripts significantly correlated with bacterial genera in healthy individuals whereas only 43 and 32 correlated with bacteria in healthy and UC siblings from discordant pairs, respectively. Several transcripts related to oxidative and immune responses were differentially expressed between unaffected and UC siblings. Conclusion. A loss of crosstalk between gut microbiota and host was highlighted in UC patients. This defect was also striking in healthy siblings from discordant pairs, as was the lower biodiversity within the microbiota. Our results suggest disease-relevant interactions between host transcriptome and microbiota. Moreover, unusual aerobic bacteria were noticed in UC mucosal microbiota, whereas healthy siblings from discordant pairs had higher percentages of potentially beneficialusual commensal bacterial species. Paired samples (twins) were analyzed to obtain data independent of genetic variation
2012-01-18 | E-GEOD-22619 | biostudies-arrayexpress
Project description:The mammalian gut is inhabited by a large and complex microbial community that lives in a mutualistic relationship with its host. Innate and adaptive mucosal defense mechanisms ensure a homeostatic relationship with this commensal microbiota. Secretory antibodies are generated from the active polymeric Ig receptor (pIgR)-mediated transport of IgA and IgM antibodies to the gut lumen and form the first line of adaptive immune defense of the intestinal mucosa. We probed mucosal homeostasis in pIgR knockout (KO) mice, which lack secretory antibodies. We found that in pIgR KO mice, colonic epithelial cells, the cell type most closely in contact with intestinal microbes, differentially expressed (>2-fold change) more than 200 genes compared with wild type mice, and upregulated the expression of anti-microbial peptides in a commensal-dependent manner. Detailed profiling of microbial communities based on 16S rRNA genes revealed differences in the commensal microbiota between pIgR KO and wild type mice. Furthermore, we found that pIgR KO mice showed increased susceptibility to dextran sulfate sodium (DSS)-induced colitis, and that this was driven by their conventional intestinal microbiota. In conclusion, secretory antibodies or the pIgR itself are required to maintain a stable commensal microbiota. In the absence of these humoral effector components, gut homeostasis is disturbed and the outcome of colitis significantly worsened. 4 groups: wild type mice treated with antibiotic (5 replicates), wild type mice left untreated (5 replicates), pIgR KO mice treated with antibiotic (6 replicates), and pIgR KO mice left untreated (6 replicates).
2013-12-28 | E-GEOD-34630 | biostudies-arrayexpress
Project description:Commensal microbiota contribute to gut homeostasis and influence mucosal gene expression. We harvested mucosal lining of middle and distal part of the small intestine and colon from germ-free (GF) and gnotobiotic mice monocolonized either with the E.coli strain O6K13 (O) or Nissle 1917 strain (N). The expression profiles of the mucosa samples were compared to the corresponding tissue isolated from conventionally reared mice in order to disclose genes differentially expressed in response to the change in the intestinal microflora composition.
2019-09-13 | E-MTAB-7726 | biostudies-arrayexpress
Project description:The indigenous human gut microbiota is a major contributor to the human superorganism with established roles in modulating nutritional status, immunity, and systemic health including diabetes and obesity. The complexity of the gut microbiota consisting of over 1012 residents and approximately 1000 species has thus far eluded systematic analyses of the precise effects of individual microbial residents on human health. In contrast, health benefits have been shown upon ingestion of certain so-called probiotic Lactobacillus strains in food products and nutritional supplements, thereby providing a unique opportunity to study the global responses of a gut-adapted microorganism in the human gut and to identify the molecular mechanisms underlying microbial modulation of intestinal physiology, which might involve alterations in the intestinal physico-chemical environment, modifications in the gut microbiota, and/or direct interaction with mucosal epithelia and immune cells. Here we show by transcriptome analysis using DNA microarrays that the established probiotic bacterium, L. plantarum 299v, adapts its metabolic capacity in the human digestive tract for carbohydrate acquisition and expression of exo-polysaccharide and proteinaceous cell surface compounds. This report constitutes the first application of global gene expression profiling of a gut-adapted commensal microorganism in the human gut. Comparisons of the transcript profiles to those obtained for L. plantarum WCFS1 in germ-free mice revealed conserved L. plantarum responses indicative of a core transcriptome expressed in the mammalian gut and provide new molecular targets for determining microbial-host interactions affecting human health. Hybridization of the samples against a common reference of gDNA isolated from L. plantarum 299v
2010-05-16 | E-GEOD-17634 | biostudies-arrayexpress
Project description:Healthy human and mouse colon epithelium is a major source of active thrombin, released in lumen. Using germ-free animals, we demonstrated that mucosal thrombin was directly regulated by the presence of commensal microbiota. Specific inhibition of lumenal thrombin activity caused macro-, microscopic damage and transcriptomic alterations of genes involved in host-microbiota interactions. Further, lumenal thrombin inhibition impaired the spatial segregation of microbiota biofilms, allowing bacteria to invade the mucus layer and to translocate across the epithelium. Thrombin proteolyzed the biofilm matrix of reconstituted mucosa-associated human microbiota. We demonstrated a previously unknown physiological role for epithelial thrombin that constrains biofilms at mucosal surfaces. We report that lung, bladder and skin epithelia also expressed thrombin, suggesting that this role may be applicable to other host-microbiome surfaces. Our discovery points route to new therapies targeting biofilms, important for a broad range of disorders, in the gut, and beyond.
2019-06-24 | PXD014315 | Pride