Foundry120 atlas

Human recipients data--Pyruvate:Ferredoxin Oxidoreductase Of Faecalibacteria prausnitzii is pro-IFN-r and Mediates Host-Microbial Crosstalk

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Dataset overview

Participants 64
Samples 64
Reuse readiness 6.7/10 evidence-backed score

Pyruvate: Ferredoxin oxidoreductase is involved in IgA-related microbiota dysbiosis and intestinal inflammation.

Abstract

<h4>Introduction</h4>Inflammatory bowel diseases (IBDs) are associated with both immune abnormalities and dysbiosis, characterized by a loss of Faecalibacterium prausnitzii (F. prausnitzii). However, the reason for F. prausnitzii deficiency remains unclear.<h4>Methods</h4>16S rDNA seque-ncing and IgA enzyme-linked immunosorbent assay (ELISA) were applied to identify bacterial community and IgA changes in ulcerative colitis (UC) patients. Forced immunization with F. prausnitzii in rabbits was conducted. To screen for potential IgA-reactive proteins in F. prausnitzii lysates, we performed western blotting and mass spectrometry analyses. Pyruvate: ferredoxin oxidoreductase (PFOR) was cloned and purified, then the immunoreactivity of PFOR was verified in peripheral blood mononuclear cells (PBMCs) through PCR, ELISpot assay and single-cell sequencing (scRNA-seq). Finally, the UC fecal dysbiosis was re-analyzed in the context of the phylogenetic tree of PFOR.<h4>Results</h4>F. prausnitzii was underrepresented in UC patients with elevated F. prausnitzii-reactive IgA in the fecal supernatant. Forced immunization with F. prausnitzii in rabbits led to high interferon-γ (IFN-γ) transcription in the colon, along with beta diversity disturbance and intestinal inflammation. PFOR was identified as an IgA-binding antigen of F. prausnitzii and the immunoreactivity was validated in PBMCs, which showed elevated expression of inflammatory cytokines. The scRNA-seq revealed enhanced signals in both T regulatory cells (Tregs) and monocytes after PFOR incubation. Furthermore, phylogenetic analysis revealed that PFOR was a common but conserved protein among the gut bacteria.<h4>Discussion</h4>Our results collectively suggest that PFOR is a bioactive protein in the immune system and may contribute to host-microbial crosstalk. Conserved but bioactive microbial proteins, such as PFOR, warrant more attention in future host-microbial interaction studies.

Study facts

Organism
—
Platform
Illumina MiSeq
Age group
—
Disease groups
Non-IBD controls, Ulcerative colitis
Anatomical sites
—

Data availability

Specific data assets have not been resolved from the source yet — see the source repository below for the full file listing.

Strengths & limitations for reuse

Strengths

  • Raw reads are advertised
  • Feature/OTU tables are advertised
  • Taxonomic tables are advertised
  • Participant counts are documented
  • Sample counts are documented
Extraction evidence & provenance

Each extracted field is shown with the source excerpt and location used to resolve it.

Assay

FieldValueEvidence
assay.paired_end True
paired-end sequencing was performed using an Illumina MiSeq PE300 system

Section Materials and methods—16S rRNA sequencing, offset 11400

assay.platform Illumina MiSeq from source
ENA instrument_model=Illumina MiSeq

Section ENA study report, offset —

assay.primers_reported True
with barcode-indexed primers (338F: 5’-ACT CCT ACG GGA GGC AGC AG-3’, 806R: 5’-ACT CCT ACG GGA GGC AGC AG-3’)

Section Materials and methods—16S rRNA sequencing, offset 11100

assay.read_length 300 inferred
paired-end sequencing was performed using an Illumina MiSeq PE300 system

Section Materials and methods—16S rRNA sequencing, offset 11400

assay.sequencing_type amplicon_16s
16S rRNA sequencing

Section Materials and methods—16S rRNA sequencing, offset 11000

Cohort

FieldValueEvidence
cohort.disease_activity_metadata_available True
Disease severity was assessed according to Mayo scores for patients with UC.

Section Materials and methods—Patients, offset 6350

cohort.non_ibd_controls 28
The human subjects included 36 UC patients and 28 healthy controls.

Section Materials and methods—Patients, offset 6100

cohort.total_participants 64
The human subjects included 36 UC patients and 28 healthy controls.

Section Materials and methods—Patients, offset 6100

cohort.ulcerative_colitis_participants 36
The human subjects included 36 UC patients and 28 healthy controls.

Section Materials and methods—Patients, offset 6100

Data_Assets

FieldValueEvidence
data_assets.feature_or_otu_table True
The abundance of the two groups at the genus level is shown in Supplementary Data 1.

Section Results—A decrease of Faecalibacterium with increased IgA responses in UC patients, offset 38000

data_assets.open_access True
"isOpenAccess": "Y"

Section Publication metadata, offset —

data_assets.raw_reads True
The data presented in the study are deposited in the NCBI repository, accession number PRJNA648093 (human microbiome)

Section Data availability statement, offset 69200

data_assets.taxonomic_table True
The abundance of the two groups at the genus level is shown in Supplementary Data 1.

Section Results—A decrease of Faecalibacterium with increased IgA responses in UC patients, offset 38000

Specimens

FieldValueEvidence
specimens.body_site gut inferred
Previous studies have documented that alterations in the gut microbiota contribute to the initiation and progression of UC

Section Introduction, offset 700

specimens.number_of_samples 64 from source
ENA sample_count=64

Section ENA study report, offset —

specimens.sample_type stool
Human fecal microbiota samples were processed at Majorbio (Shanghai, China).

Section Materials and methods—16S rRNA sequencing, offset 11000