Human gut metagenome
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA493203 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR7985060_1.fastq.gz | Fastqsanger.gz | |||
| SRR7985060_2.fastq.gz | Fastqsanger.gz | |||
| SRR7985070_1.fastq.gz | Fastqsanger.gz | |||
| SRR7985070_2.fastq.gz | Fastqsanger.gz | |||
| SRR7985061_1.fastq.gz | Fastqsanger.gz |
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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).
2013-12-28 | E-GEOD-34630 | biostudies-arrayexpress
Project description:16S rRNA amplicon sequencing from human feces and the Simulator of Human Intestinal Microbial Ecosystem (SHIME) Raw sequence reads
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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
Project description:Enterocyte Iron Mucosal Block
This is a model of enterocyte iron absorption, consisting of iron uptake (movement of iron from intestinal lumen into cytplasm), and transfer (transport of iron from cytoplasm to blood/plasma). The model was created by Joseph Masison and Pedro Mendes.
Intestinal mucosal block is a cellular phenomenon defined by a transient reduction in iron absorption by intestinal epithelial cells following previous iron exposures. Understanding what controls the mucosal block is central to understanding how intestinal iron absorption contributes to pathological iron states. Three mechanisms implicated in driving mucosal block are the endocytosis of divalent metal transporter 1 (DMT1), sequestration of iron by cytosolic ferritin, and iron regulatory proteins (IRPs) regulation of ferritin expression.
Here, we build a model that reproduces the mucosal block phenomena, based on published experimental data, and use it to quantify the contribution of each mechanism to the block. Model analysis shows ferritin and IRPs regulation have the largest quantitative impact on the mucosal block. Lastly, DMT1 endocytosis is shown to play a role in limiting total enterocyte iron uptake, protecting the cell against oxidative stress, but does not contribute to the decrease in total iron transfer seen in mucosal block.
CC0 1.0 Universal: To the extent possible under law, all copyright and related or neighbouring rights to this encoded model have been dedicated to the public domain worldwide. You can copy, modify, distribute and perform the work, even for commercial purposes, all without asking permission. Please refer to CC0 Public Domain Dedication for more information.
2025-02-11 | MODEL2405170001 | BioModels
Project description:Transfer of antibiotic resistance plasmid from commensal E. coli towards human intestinal microbiota in the M-SHIME: influence of E. coli dosis, human individual and antibiotic use
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Project description:The most clinically relevant risk factor for Clostridioides difficile-associated disease (CDAD) is recent antibiotic treatment. Though most broad-spectrum antibiotics significantly disrupt the structure of the gut microbiota, only particular ones increase CDAD risk, suggesting additional factors might increase the risk from certain antibiotics. Here we show that commensal-independent effects of antibiotics collectively prime an in vitro germ-free human gut for CDAD. We found a marked loss of mucosal barrier and immune function with CDAD-associated antibiotic pretreatment distinct from pretreatment with an antibiotic unassociated with CDAD, which did not reduce innate immune or mucosal barrier functions. Importantly, pretreatment with CDAD-associated antibiotics sensitized mucosal barriers to C. difficile toxin activity in primary cell-derived enteroid monolayers. These data implicate commensal-independent host changes in the increased risk of CDAD with specific antibiotics. Our findings are contrary to the previously held belief that antibiotics allow for CDAD solely through disruption of the microbiome. We anticipate this work to suggest potential avenues of research for host-directed treatment and preventive therapies for CDAD, and to impact human tissue culturing protocols.
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Project description:Alteration of transit time in the Simulator of the Human Intestinal Microbial Ecosystem
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Project description:Adaptation of transit time in the Simulator of the Human Intestinal Microbial Ecosystem
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Project description:Antibiotic resistance is exacerbated by the exchange of antibiotic resistance genes (ARGs) between microbes from diverse habitats. Plasmids are important ARGs mobile elements and are spread by horizontal gene transfer (HGT). In this study, we demonstrated the presence of multi-resistant plasmids from inhalable particulate matter (PM) and its effect on gene horizontal transfer. Three transferable multi-resistant plasmids were identified from PM in a hospital, using conjugative mating assays and nanopore sequencing. pTAir-3 contained 26 horizontal transfer elements and 10 ARGs. Importantly pTAir-5 harbored carbapenem resistance gene (blaOXA) which shows homology to plasmids from human and pig commensal bacteria, thus indicating that PM is a media for antibiotic resistant plasmid spread. In addition, 125 μg/mL PM2.5 and PM10 significantly increased the conjugative transfer rate by 110% and 30%, respectively, and augmented reactive oxygen species (ROS) levels. Underlying mechanisms were revealed by identifying the upregulated expressional levels of genes related to ROS, SOS, cell membranes, pilus generation, and transposition via genome-wide RNA sequencing. The study highlights the airborne spread of multi-resistant plasmids and the impact of inhalable PM on the horizontal transfer of antibiotic resistance.
2022-10-31 | GSE159850 | GEO