Enterococcus gallinarum
This sample represents a Third Party Annotation (TPA) Metagenome-Assembled Genome (MAG) assembled from the metagenomic run SRR18243789 of study SRP362674.
ENA-FIRST-PUBLIC
2022-12-17
ENA-LAST-UPDATE
2022-12-17
External Id
SAMEA112250219
INSDC center alias
EMG
INSDC center name
EMG
INSDC first public
2022-12-17T00:47:18Z
INSDC last update
2022-12-17T00:47:18Z
INSDC status
public
Submitter Id
SRR18243789_bin.5_metawrap_v1.3_MAG
assembly quality
Many fragments with little to no review of assembly other than reporting of standard assembly statistics
assembly software
not provided
binning parameters
MaxBin2, MetaBat2, Concoct with default parameter of the metaWRAP pipeline. Bin refinement module used from metaWRAP with default parameters.
binning software
metawrap v1.3
broad-scale environmental context
mouse digestive system
broker name
EMG broker account, EMBL-EBI
collection date
2015-12-21
completeness score
98.13
completeness software
CheckM
contamination score
0.0
environmental medium
feces
geographic location (country and/or sea)
Germany
geographic location (latitude)
52.62686
geographic location (longitude)
13.507567
investigation type
metagenome-assembled genome
isolation_source
mouse gut metagenome
local environmental context
digestive tube
metagenomic source
mouse gut metagenome
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.&lt;/p&gt;&lt;p&gt;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.&lt;/p&gt;&lt;p&gt;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.
sample derived from
SAMN26378646
sample name
SRR18243789_bin.5_metawrap_v1.3_MAG
sequencing method
Illumina NovaSeq 6000
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__Bacilli;o__Lactobacillales;f__Enterococcaceae;g__Enterococcus;s__Enterococcus gallinarum
taxonomic identity marker
multi-marker approach