Metagenome-assembled genome: SRR19759449_bin.45_metawrap_v1.3_MAG
uncultured Hungatella sp.
ENA-FIRST-PUBLIC
2022-12-12
ENA-LAST-UPDATE
2022-12-12
External Id
SAMEA112223372
INSDC center alias
EMG
INSDC center name
EMG
INSDC first public
2022-12-12T16:30:06Z
INSDC last update
2022-12-12T16:30:06Z
INSDC status
public
Submitter Id
SRR19759449_bin.45_metawrap_v1.3_MAG
assembly quality
Many fragments with little to no review of assembly other than reporting of standard assembly statistics
assembly software
metaSPAdes v3.15.3
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
not provided
completeness score
93.04
completeness software
CheckM
contamination score
0.0
environmental medium
feces
geographic location (country and/or sea)
not provided
geographic location (latitude)
not provided
geographic location (longitude)
not provided
investigation type
metagenome-assembled genome
isolation_source
mouse gut metagenome
local environmental context
digestive tube
metagenomic source
mouse gut metagenome
project name
A growing body of evidence supports the notion that the gut microbiome plays an important role in cancer immunity. However, the underpinning mechanisms remain to be fully elucidated. One attractive hypothesis envisages that among the T cells elicited by the plethora of microbiome proteins a few exist that incidentally recognize neo-epitopes arising from cancer mutations (molecular mimicry (MM) hypothesis). To support MM, the human probiotic Escherichia coli Nissle was engineered with the SIINFEKL epitope (OVA-E.coli Nissle) and orally administered to C57BL6 mice. The treatment with OVA-E.coli Nissle, but not with wild type E. coli Nissle, induced OVA-specific CD8+ T cells and inhibited the growth of tumors in mice challenged with B16F10 melanoma cells expressing OVA. The microbiome shotgun sequencing and the sequencing of TCRs from T cells recovered from both lamina propria and tumors provide evidence that the main mechanism of tumor inhibition is mediated by the elicitation at the intestinal site of cross-reacting T cells, which subsequently reach the tumor environment. Importantly, the administration of Outer Membrane Vesicles (OMVs) from engineered E. coli Nissle, as well as from E. coli BL21(DE3)DompA, carrying cancer-specific T cell epitopes also elicited epitope-specific T cells in the intestine and inhibited tumor growth. Overall, our data strengthen the important role of MM in tumor immunity and assign a novel function of OMVs in host-pathogen interaction. Moreover, our results pave the way to the exploitation of probiotics and OMVs engineered with tumor specific-antigens as personalized mucosal cancer vaccines.
sample derived from
SAMN29213114
sample name
SRR19759449_bin.45_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__Clostridia;o__Clostridiales;f__Clostridiaceae;g__Hungatella;s__
taxonomic identity marker
multi-marker approach