Gut microbiome and intestinal inflammation in preclinical stages of rheumatoid arthritis.

Autoimmune Diseases Autoimmunity Permeability Rheumatoid Arthritis Rheumatoid Factor

Journal

RMD open
ISSN: 2056-5933
Titre abrégé: RMD Open
Pays: England
ID NLM: 101662038

Informations de publication

Date de publication:
30 Jan 2024
Historique:
received: 08 08 2023
accepted: 15 01 2024
medline: 1 2 2024
pubmed: 1 2 2024
entrez: 31 1 2024
Statut: epublish

Résumé

Faecal First-degree relatives of patients with RA (RA-FDRs) from the SCREEN-RA cohort were categorised into four groups: controls, healthy asymptomatic RA-FDRs; high genetic risk, asymptomatic RA-FDRs with two copies of the shared epitope; autoimmunity, asymptomatic RA-FDRs with RA-associated autoimmunity; and symptomatic, clinically suspect arthralgias or untreated new-onset RA.Faecal samples were collected and frozen. 16S sequencing was performed, processed with DADA2 pipeline and Silva database. Cell counts (cytometry) and faecal calprotectin (enzyme-linked immunosorbent assay, ELISA) were also obtained. Microbial community analyses were conducted using non-parametric tests, such as permutational multivariate analysis of variance (PERMANOVA), Wilcoxon and Kruskal-Wallis, or Aldex2. A total of 371 individuals were included and categorised according to their preclinical stage of the disease. Groups had similar age, gender and body mass index. We found no significant differences in the quantitative microbiome profiles by preclinical stages (PERMANOVA, R2=0.00798, p=0.56) and, in particular, no group differences in We could not identify microbiome profiles associated with preclinical stages of RA. Only in a subgroup of individuals with the most pronounced phenotypes did we modestly retrieve the previously reported associations.

Sections du résumé

BACKGROUND BACKGROUND
Faecal
METHODS METHODS
First-degree relatives of patients with RA (RA-FDRs) from the SCREEN-RA cohort were categorised into four groups: controls, healthy asymptomatic RA-FDRs; high genetic risk, asymptomatic RA-FDRs with two copies of the shared epitope; autoimmunity, asymptomatic RA-FDRs with RA-associated autoimmunity; and symptomatic, clinically suspect arthralgias or untreated new-onset RA.Faecal samples were collected and frozen. 16S sequencing was performed, processed with DADA2 pipeline and Silva database. Cell counts (cytometry) and faecal calprotectin (enzyme-linked immunosorbent assay, ELISA) were also obtained. Microbial community analyses were conducted using non-parametric tests, such as permutational multivariate analysis of variance (PERMANOVA), Wilcoxon and Kruskal-Wallis, or Aldex2.
RESULTS RESULTS
A total of 371 individuals were included and categorised according to their preclinical stage of the disease. Groups had similar age, gender and body mass index. We found no significant differences in the quantitative microbiome profiles by preclinical stages (PERMANOVA, R2=0.00798, p=0.56) and, in particular, no group differences in
CONCLUSIONS CONCLUSIONS
We could not identify microbiome profiles associated with preclinical stages of RA. Only in a subgroup of individuals with the most pronounced phenotypes did we modestly retrieve the previously reported associations.

Identifiants

pubmed: 38296308
pii: rmdopen-2023-003589
doi: 10.1136/rmdopen-2023-003589
pmc: PMC10836359
pii:
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Informations de copyright

© Author(s) (or their employer(s)) 2024. Re-use permitted under CC BY. Published by BMJ.

Déclaration de conflit d'intérêts

Competing interests: None declared.

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Auteurs

Benoît Thomas P Gilbert (BTP)

Division of Rheumatology, HUG, Geneva, Switzerland benoit.gilbert@unige.ch.
Geneva Centre for Inflammation Research, UNIGE, Geneva, Switzerland.

Raul Yhossef Tito Tadeo (RYT)

KU Leuven, Department of Microbiology, Immunology, and Transplantation, Rega Institute for Medical Research, B-3000 Leuven, Belgium.
VIB, Center for Microbiology, B-3000 Leuven, Belgium.

Celine Lamacchia (C)

Division of Rheumatology, HUG, Geneva, Switzerland.
Geneva Centre for Inflammation Research, UNIGE, Geneva, Switzerland.

Olivia Studer (O)

Division of Rheumatology, HUG, Geneva, Switzerland.
Geneva Centre for Inflammation Research, UNIGE, Geneva, Switzerland.

Delphine Courvoisier (D)

Division of Rheumatology, HUG, Geneva, Switzerland.
Geneva Centre for Inflammation Research, UNIGE, Geneva, Switzerland.

Jeroen Raes (J)

KU Leuven, Department of Microbiology, Immunology, and Transplantation, Rega Institute for Medical Research, B-3000 Leuven, Belgium.
VIB, Center for Microbiology, B-3000 Leuven, Belgium.

Axel Finckh (A)

Division of Rheumatology, HUG, Geneva, Switzerland.
Geneva Centre for Inflammation Research, UNIGE, Geneva, Switzerland.

Classifications MeSH