PMID- 33973546
OWN - NLM
STAT- MEDLINE
DCOM- 20211015
LR  - 20230829
IS  - 1531-6963 (Electronic)
IS  - 1040-8711 (Linking)
VI  - 33
IP  - 4
DP  - 2021 Jul 1
TI  - Intestinal dysbiosis in spondyloarthritis - chicken or egg?
PG  - 341-347
LID - 10.1097/BOR.0000000000000800 [doi]
AB  - PURPOSE OF REVIEW: The well-established link between intestinal inflammation and 
      spondyloarthritis (SpA) remains largely unexplained. Recent sequencing 
      technologies have given access to a thorough characterization of the gut 
      microbiota in healthy and disease conditions. This showed that inflammatory bowel 
      disease (IBD) is associated with dysbiosis - i.e., disturbed gut microbiota 
      composition - which may contribute to disease pathogenesis. Whether gut dysbiosis 
      exists in SpA and could contribute to disease development or be a bystander 
      consequence of chronic inflammation is a question of major interest. RECENT 
      FINDINGS: Several metagenomic studies have been performed in SpA. Most of them 
      concerned faecal samples and showed dysbiosis consisting in a reduction of 
      microbial biodiversity in a way similar to what has been described in IBD. They 
      also highlighted changes in microbial taxa composition that could contribute to 
      the inflammatory process. Likewise, healthy carriers of human leukocyte antigen 
      (HLA)-B27 exhibited gut dysbiosis, indicating that this predisposing allele could 
      exert its pathogenic effect by influencing microbiota composition, and possibly 
      by driving antigen-specific cross-reactive immune response. On the other hand, 
      SpA treatments were associated with a reduction of dysbiosis, showing that it is 
      at least in part a consequence of inflammation. SUMMARY: Recent insights from 
      metagenomic studies warrant further investigations to identify the mechanisms by 
      which microbial dysbiosis could contribute to SpA development. This would bring 
      novel therapeutic opportunities aiming at correcting detrimental changes.
CI  - Copyright (c) 2021 Wolters Kluwer Health, Inc. All rights reserved.
FAU - Breban, Maxime
AU  - Breban M
AD  - Infection & Inflammation, UMR 1173, Inserm, UVSQ/Universite Paris Saclay, 
      Montigny-le-Bretonneux.
AD  - Service de Rhumatologie, Hopital Ambroise Pare, AP-HP, Boulogne.
AD  - Laboratoire d'Excellence Inflamex, Universite Paris Descartes, Sorbonne Paris 
      Cite, Paris, France.
FAU - Beaufrere, Marie
AU  - Beaufrere M
AD  - Infection & Inflammation, UMR 1173, Inserm, UVSQ/Universite Paris Saclay, 
      Montigny-le-Bretonneux.
AD  - Service de Rhumatologie, Hopital Ambroise Pare, AP-HP, Boulogne.
AD  - Laboratoire d'Excellence Inflamex, Universite Paris Descartes, Sorbonne Paris 
      Cite, Paris, France.
FAU - Glatigny, Simon
AU  - Glatigny S
AD  - Infection & Inflammation, UMR 1173, Inserm, UVSQ/Universite Paris Saclay, 
      Montigny-le-Bretonneux.
AD  - Laboratoire d'Excellence Inflamex, Universite Paris Descartes, Sorbonne Paris 
      Cite, Paris, France.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Review
PL  - United States
TA  - Curr Opin Rheumatol
JT  - Current opinion in rheumatology
JID - 9000851
RN  - 0 (HLA-B27 Antigen)
SB  - IM
MH  - Dysbiosis
MH  - *Gastrointestinal Microbiome
MH  - HLA-B27 Antigen
MH  - Humans
MH  - *Inflammatory Bowel Diseases
MH  - *Spondylarthritis
EDAT- 2021/05/12 06:00
MHDA- 2021/10/16 06:00
CRDT- 2021/05/11 09:27
PHST- 2021/05/12 06:00 [pubmed]
PHST- 2021/10/16 06:00 [medline]
PHST- 2021/05/11 09:27 [entrez]
AID - 00002281-202107000-00007 [pii]
AID - 10.1097/BOR.0000000000000800 [doi]
PST - ppublish
SO  - Curr Opin Rheumatol. 2021 Jul 1;33(4):341-347. doi: 10.1097/BOR.0000000000000800.