Arthritis Research & Therapy (Jul 2022)

Distinctive gut microbiomes of ankylosing spondylitis and inflammatory bowel disease patients suggest differing roles in pathogenesis and correlate with disease activity

  • P. R. Sternes,
  • L. Brett,
  • J. Phipps,
  • F. Ciccia,
  • T. Kenna,
  • E. de Guzman,
  • K. Zimmermann,
  • M. Morrison,
  • G. Holtmann,
  • E. Klingberg,
  • D. Mauro,
  • C. McIvor,
  • H. Forsblad-d’Elia,
  • M. A. Brown

DOI
https://doi.org/10.1186/s13075-022-02853-3
Journal volume & issue
Vol. 24, no. 1
pp. 1 – 10

Abstract

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Abstract Background Multiple studies have confirmed dysbiosis in ankylosing spondylitis (AS) and inflammatory bowel disease (IBD); however, due to methodological differences across studies, it has not been possible to determine if these diseases have similar or different gut microbiomes. Results In this study, faecal and intestinal biopsies were obtained from 33 Australian AS patients (including 5 with concomitant IBD, ‘AS-IBD’), 59 IBD patients and 105 healthy controls. Stool samples were also obtained from 16 Italian AS patients and 136 Swedish AS patients. Focusing on the Australian cohort, AS, AS-IBD and IBD patients differed from one another and from healthy controls in both alpha and beta diversity. AS patients with and without clinical IBD could be distinguished from one another with moderate accuracy using stool microbiome (AUC=0.754). Stool microbiome also accurately distinguished IBD patients from healthy controls (AUC=0.757). Microbiome composition was correlated with disease activity measured by BASDAI and faecal calprotectin (FCP) levels. Enrichment of potentially pathogenic Streptococcus was noted in AS, AS-IBD and IBD patients. Furthermore, enrichment of another potentially pathogenic genus, Haemophilus, was observed in AS, AS-IBD, IBD, AS patients with increased BASDAI, and IBD patients with faecal calprotectin >100 μg/mg. Apart from these genera, no other taxa were shared between AS and IBD patients. Conclusions In conclusion, the distinct gut microbiome of AS and AS-IBD patients compared to IBD patients and healthy controls is consistent with immunological and genetic evidence suggesting that the gut plays a different role in driving AS compared with IBD. However, enrichment of two potentially pathogenic genera in both diseases suggests that the presence of a shared/common microbial trigger of disease cannot be discounted.

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