Table 1 ∣.
Disease | Study design | Intervention | Result | Ref. |
---|---|---|---|---|
Ulcerative colitis | Prospective | TNF inhibitors | Non-responders characterized by high dysbiosis indices and a lower abundance of Faecalibacterium prausnitzii at baseline | 80 |
Ulcerative colitis and Crohn’s disease | Prospective | Vedolizumab | High microbial diversity at baseline, specific taxa (e.g. Roseburia inulinivorans) and several microbial pathways enriched in patients achieving remission | 81 |
Crohn’s disease | Prospective | Ustekinumab | Patients achieving remission had high microbial diversity and enrichment of specific taxa at baseline | 82 |
Axial SpA | Prospective | TNF inhibitors | High relative abundance of the order Burkholderiales at baseline was modestly predictive of future response | 92 |
PsA and SpA | Prospective | TNF and IL-17A inhibitors | Abundance of several specific taxa (e.g. Clostridiales) shifted after treatment with IL-17 blockade (as compared with TNF inhibition); Candida albicans was expanded in a subset of patients following IL-17 blockade | 94 |
Treatment-naive, chronic RA | Prospective | Herbal remedies with or without methotrexate | Oral microbiome (and to a lesser degree the gut microbiome) distinguished responders from non-responders | 126 |
Treatment-naive, new-onset RA | Prospective | Methotrexate | Gut metagenome at baseline could differentiate methotrexate responders from non-responders; ex vivo incubation with methotrexate of samples from patients with treatment-naive, new-onset RA correlated with the magnitude of future clinical response | 129 |
PsA, psoriatic arthritis; RA rheumatic arthritis; SpA, spondyloarthritis.