2025-10-10
ENA first public
ERC000047
ENA-CHECKLIST
EMG
INSDC center name
public
INSDC status
ERS26977707
SRA accession
SRR25744291_concoct_15
Submitter Id
Many fragments with little to no review of assembly other than reporting of standard assembly statistics
assembly quality
metaspades_v3.15.5
assembly software
default
binning parameters
MGnify-genomes-generation-pipeline_v1.2.0
binning software
human digestive system
broad-scale environmental context
EBI-EMG
broker name
2020
collection date
99.19
%
completeness score
CheckM2_v1.0.1
completeness software
0.01
%
contamination score
This sample represents a Third Party Annotation (TPA) Metagenome-assembled genome assembled from the metagenomic run SRR25744291 of study SRP456718.
description
subgingival plaque
environmental medium
USA
geographic location (country and/or sea)
38.59000000
DD
geographic location (latitude)
-77.60000000
DD
geographic location (longitude)
metagenome-assembled genome
investigation type
human oral metagenome
isolation_source
oral cavity
local environmental context
human oral metagenome
metagenomic source
Tannerella forsythia
organism
Mucosal surfaces protect the host from the external environment by providing a physical barrier and an innate anti-microbial defense system. At mucosal barriers, while commensal microbiota plays an integral role in the regulation of homeostatic epithelial barrier responses, microbial dysbiosis is linked to dysregulation of barrier immunity. Here, in the context of the prevalent oral mucosal disease periodontitis, we describe a mechanism by which shifts in microbial communities trigger a proinflammatory epithelial response and promote immunopathology. In this Th17-mediated oral inflammatory disease, IL-23, the upstream regulator of Th17 disease expansion, is expressed within the epithelium, proximal to the disease-associated microbiome, both in experimental models and in patients with common and Mendelian forms of disease. In contrast to many other Th17-driven pathologies, in periodontitis, non-hematopoietic cell-derived IL-23 triggers pathogenic inflammation and tissue destruction. Specifically, flagellated microbial species, which are predominant constituents of the disease microbiome in periodontitis, trigger induction of epithelial IL-23, in a TLR5-dependent manner. Analysis of publicly available datasets, further supports expression of epithelial IL-23 in diverse tissue microenvironments with significant expansion in particular settings of inflammation, malignancy, and autoimmunity, suggesting a broader role for epithelial-derived IL-23 in barrier disease pathology. Collectively, this work ties together, sensing of pathobionts with the induction of pathogenic inflammation and reveals a primary role for the epithelium in mucosal disease triggering.
project name
SAMN37047878
sample derived from
Tannerella forsythia
scientific_name
NextSeq 500
sequencing method
multi-marker approach
taxonomic identity marker
Metagenome-assembled genome: SRR25744291_concoct_15
title