NOD2 influences intestinal microbial resilience after antibiotic perturbation

Dataset overview

Participants None

Samples 2

Reuse readiness 6.1/10 evidence-backed score

NOD2 Influences Trajectories of Intestinal Microbiota Recovery After Antibiotic Perturbation.

Moltzau Anderson J, Lipinski S, Sommer F, Pan WH, Boulard O, Rehman A, Falk-Paulsen M, Stengel ST, et al. · Cellular and molecular gastroenterology and hepatology · 2020

Abstract

<h4>Background & aims</h4>Loss-of-function variants in nucleotide-binding oligomerization domain-containing protein 2 (NOD2) impair the recognition of the bacterial cell wall component muramyl-dipeptide and are associated with an increased risk for developing Crohn's disease. Likewise, exposure to antibiotics increases the individual risk for developing inflammatory bowel disease. Here, we studied the long-term impact of NOD2 on the ability of the gut bacterial and fungal microbiota to recover after antibiotic treatment.<h4>Methods</h4>Two cohorts of 20-week-old and 52-week-old wild-type (WT) C57BL/6J and NOD2 knockout (Nod2-KO) mice were treated with broad-spectrum antibiotics and fecal samples were collected to investigate temporal dynamics of the intestinal microbiota (bacteria and fungi) using 16S ribosomal RNA and internal transcribed spacer 1 sequencing. In addition, 2 sets of germ-free WT mice were colonized with either WT or Nod2-KO after antibiotic donor microbiota and the severity of intestinal inflammation was monitored in the colonized mice.<h4>Results</h4>Antibiotic exposure caused long-term shifts in the bacterial and fungal community composition. Genetic ablation of NOD2 was associated with delayed body weight gain after antibiotic treatment and an impaired recovery of the bacterial gut microbiota. Transfer of the postantibiotic fecal microbiota of Nod2-KO mice induced an intestinal inflammatory response in the colons of germ-free recipient mice compared with respective microbiota from WT controls based on histopathology and gene expression analyses.<h4>Conclusions</h4>Our data show that the bacterial sensor NOD2 contributes to intestinal microbial community composition after antibiotic treatment and may add to the explanation of how defects in the NOD2 signaling pathway are involved in the etiology of Crohn's disease.

doi:10.1016/j.jcmgh.2020.03.008 ↗ PMID 32289499 ↗ PMC7327897 ↗

Study facts

Organism: —
Platform: Illumina MiSeq
Age group: adult
Disease groups: —
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
Sample counts are documented

Limitations

Not documented: participant counts are documented

Extraction evidence & provenance

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

Assay

Field	Value	Evidence
`assay.paired_end`	True	Samples were pooled and paired-end sequenced (2 × 300 base pairs) on an Illumina MiSeq. Section `Fungal ITS1 Amplicon Sequencing`, offset 114000
`assay.platform`	Illumina MiSeq from source	ENA instrument_model=Illumina MiSeq Section `ENA study report`, offset —
`assay.primers_reported`	True	the primers ITS1-F(F) ... and ITS2(R) ... to amplify the fungal ITS1 region Section `Fungal ITS1 Amplicon Sequencing`, offset 112500
`assay.read_length`	300	paired-end sequenced (2 × 300 base pairs) Section `Fungal ITS1 Amplicon Sequencing`, offset 114000

Cohort

Field	Value	Evidence
`cohort.age_group`	adult	We thus performed a short-term antibiotic combination therapy ... in adult mice Section `Introduction`, offset 3500
`cohort.study_design`	longitudinal	to investigate the effect of NOD2 on longitudinal dynamics of the bacterial microbiota Section `Introduction`, offset 3600
`cohort.treatment_exposure_documented`	True	SPF C57BL/6J WT and Nod2 -KO mice were treated with a cocktail of broad-spectrum antibiotics Section `Antibiotic Treatment`, offset 103000
`cohort.treatment_response_metadata_available`	True	animals lost substantial weight ... Recovery from antibiotic-induced weight loss occurred earlier and faster in WT mice Section `Results`, offset 7000

Data_Assets

Field	Value	Evidence
`data_assets.feature_or_otu_table`	True	to generate an OTU abundance table Section `Fungal ITS1 Amplicon Sequencing`, offset 114800
`data_assets.open_access`	True from source	"isOpenAccess": "Y" Section `Publication metadata`, offset —
`data_assets.pipeline_or_tool_versions`	True	using Mothur and MacQIIME v1.9.1 Section `16S Amplicon Sequencing`, offset 109300
`data_assets.qc_or_negative_controls_reported`	True	Sequences ... were considered for further alignment ... Chimeric sequences ... were removed Section `16S Amplicon Sequencing`, offset 109000
`data_assets.raw_reads`	True	Raw sequencing data ... were uploaded to ... ENA under accession number PRJEB21817 Section `Availability of Data and Materials`, offset 125000
`data_assets.taxonomic_table`	True	used to assign taxonomic classifications ... and to generate an OTU abundance table Section `Fungal ITS1 Amplicon Sequencing`, offset 114700

Specimens

Field	Value	Evidence
`specimens.body_site`	feces	Fecal pellets were collected immediately from mice throughout the experiment Section `Specific Pathogen–Free Mice`, offset 101000
`specimens.longitudinal_sampling`	True	16S rRNA gene amplicon sequencing was performed on longitudinally sampled fecal material Section `16S Amplicon Sequencing`, offset 108000
`specimens.number_of_samples`	2 from source	ENA sample_count=2 Section `ENA study report`, offset —
`specimens.sample_type`	stool	DNA from fecal pellets was isolated using the PowerSoil DNA Isolation Kit Section `16S Amplicon Sequencing`, offset 108000