| broad-scale environmental context | mouse digestive system |
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| collection date | 2016-03-24 |
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| environmental medium | feces |
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| geographic location | Germany |
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| investigation type | metagenome-assembled genome |
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| isolation source | mouse gut metagenome |
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| project name | Hypertension (HTN) can lead to heart and kidney damage. The gut microbiota has been linked to HTN, although it is difficult to estimate its significance due to the variety of other features known to influence HTN. In the present study, we used germ-free (GF) and colonized (COL) littermate mice to quantify the impact of microbial colonization on organ damage in HTN.</p><p>Four-week-old male GF C57BL/6J littermates were randomized to remain GF or receive microbial colonization. HTN was induced by subcutaneous infusion with angiotensin (Ang) II (1.44mg/kg/d) and 1% NaCl in the drinking water; sham-treated mice served as control. Renal damage was exacerbated in GF mice, whereas cardiac damage was more comparable between COL and GF, suggesting that the kidney is more sensitive to microbial influence. Multivariate analysis revealed a larger effect of HTN in GF mice. Serum metabolomics demonstrated that the colonization status influences circulating metabolites relevant to HTN. Importantly, GF mice were deficient in anti-inflammatory fecal short-chain fatty acids (SCFA). Flow cytometry showed that the microbiome has an impact on the induction of anti-hypertensive myeloid-derived suppressor cells and pro-inflammatory Th17 cells in HTN. In vitro inducibility of Th17 cells was significantly higher for cells isolated from GF than conventionally raised mice.</p><p>Microbial colonization status of mice had potent effects on their phenotypic response to a hypertensive stimulus, and the kidney is a highly microbiota-susceptible target organ in HTN. The magnitude of the pathogenic response in GF mice underscores the role of the microbiome in mediating inflammation in HTN. |
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| sample name | SRR18243806_bin.1_metawrap_v1.3_MAG |
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| ENA-CHECKLIST | ERC000047 |
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| ENA-FIRST-PUBLIC | 2022-12-17 |
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| ENA-LAST-UPDATE | 2022-12-17 |
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| External Id | SAMEA112250366 |
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| INSDC center alias | EMG |
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| INSDC center name | EMG |
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| INSDC first public | 2022-12-17T00:47:18Z |
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| INSDC last update | 2022-12-17T00:47:18Z |
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| INSDC status | public |
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| Submitter Id | SRR18243806_bin.1_metawrap_v1.3_MAG |
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| assembly quality | Many fragments with little to no review of assembly other than reporting of standard assembly statistics |
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| assembly software | metaSPAdes v3.15.3 |
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| binning parameters | MaxBin2, MetaBat2, Concoct with default parameter of the metaWRAP pipeline. Bin refinement module used from metaWRAP with default parameters. |
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| binning software | metawrap v1.3 |
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| broker name | EMG broker account, EMBL-EBI |
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| completeness score | 98.85 |
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| completeness software | CheckM |
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| contamination score | 2.39 |
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| geographic location (latitude) | 52.62686 |
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| geographic location (longitude) | 13.507567 |
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| local environmental context | digestive tube |
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| metagenomic source | mouse gut metagenome |
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| sample derived from | SAMN26378630 |
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| sequencing method | Illumina NovaSeq 6000 |
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| taxonomic classification | The taxonomy of this metagenome-assembled genome was originally computed with GTDBtk, which assigned the following taxonomic annotation: d__Bacteria;p__Firmicutes;c__Clostridia;o__Clostridiales;f__Lachnospiraceae;g__;s__ |
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| taxonomic identity marker | multi-marker approach |
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