Feces metagenome
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA355065 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR5056050.fastq.gz | Fastqsanger.gz | |||
| SRR5056041.fastq.gz | Fastqsanger.gz | |||
| SRR5056051.fastq.gz | Fastqsanger.gz | |||
| SRR5056042.fastq.gz | Fastqsanger.gz | |||
| SRR5056052.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 13 |
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Project description:We compared gut microbiota of IFI16 KO and WT mice by 16s sequencing
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Project description:Ulcerative colitis (UC) is an intestinal pathology characterized by chronic recurrent inflammation, which requires in-depth exploration of its mechanisms. To investigate the biological effects of TLR2 on DSS-induced intestinal inflammation in mice, we constructed the WT and TLR2-KO colitis mice model. We found TLR2-KO mice were severely susceptible to DSS-induced colitis. To determine how TLR2 exerted a protective effect in DSS-induced colitis, we compared the global gene expression profiles in the gut between WT and TLR2-KO mice by RNA-Seq. Results suggested that cell cycle pathway-related genes were significantly downregulated in gut of TLR2-KO colitis mice. 16S rRNA gene sequencing demonstrated remarkable variation in the composition of gut microbiota between WT and TLR2-KO colitis mice. Compared with WT colitis mice, the relative abundance of Marinifilaceae, Rikenellaceae, Desulfovibrionaceae, Tannerellaceae, Ruminococcaceae, Clostridia, Mycoplasmataceae were significantly higher in the gut of TLR2-KO colitis mice at family level. Moreover, we found that the relative abundance of Marinifilaceae was negatively correlated with the expression of cell cycle signaling related genes by microbiome diversity-transcriptome collaboration analysis. We came to this conclusion: TLR 2-KO exacerbated DSS-induced intestinal injury by Marinifilaceae dependent attenuating cell cycle signaling.
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Project description:This study aimed to analyze changes in gut microbiota composition in mice after transplantation of fecal microbiota (FMT, N = 6) from the feces of NSCLC patients by analyzing fecal content using 16S rRNA sequencing, 10 days after transplantation. Specific-pathogen-free (SPF) mice were used for each experiments (N=4) as controls.
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Project description:Abstract. Background: The cause of ulcerative colitis (UC) is not yet fully understood. Previous research has pointed towards a potential role for mutations in NOD2 in promoting the onset and progression of inflammatory bowel disease (IBD) by altering the microbiota of the gut. However, the relationship between toll-like receptor 4 (TLR4) and gut microbiota in IBD is not well understood. To shed light on this, the interaction between TLR4 and gut microbiota was studied using a mouse model of IBD. Methods: To examine the function of TLR4 signaling in intestinal injury repair, researchers developed Dextran Sulfate Sodium Salt (DSS)-induced colitis and injury models in both wild-type (WT) mice and TLR4 knockout (TLR4-KO) mice. To assess changes in the gut microbiota, 16S rRNA sequencing was conducted on fecal samples from both the TLR4-KO and WT enteritis mouse models. Results: The data obtained depicted a protective function of TLR4 against DSS-induced colitis. The gut microbiota composition was found to vary considerably between the WT and TLR4-KO mice groups as indicated by β-diversity analysis and operational taxonomic units (OTUs) cluster. Statistical analysis of microbial multivariate variables depicted an elevated abundance of Escherichia coli/Shigella, Gammaproteobacteria, Tenerlcutes, Deferribacteres, Enterobacteria, Rikenellaceae, and Proteobacteria in the gut microbiota of TLR4-KO mice, whereas there was a considerable reduction in Bacteroidetes at five different levels of the phylogenetic hierarchy including phylum, class, order, family, and genus in comparison with the WT control. Conclusion: TLR4 may protect intestinal epithelial cells from damage in response to DSS-induced injury by controlling the microbiota in the gut.
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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).
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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.
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Project description:We compared gut microbiota of mir-21 KO and WT mice by 16s sequencing
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