Autoinflammatory & rare systemic diseases

Gut microbiota alterations are associated with phenotype and genotype in familial Mediterranean fever

Rheumatology (Oxford)Published Cross-sectional study

Authors' conclusion

The gut microbiota of FMF patients correlates with disease characteristics and severity, with an increase in pro-inflammatory taxa in the most severe patients.

Study context

Population
Large cohort of FMF patients (AA amyloidosis n = 17, hepatopathy n = 5, colchicine resistance n = 27, biotherapy n = 10) and healthy controls
Participants
119 vs 61
Exposure
FMF patients vs healthy controls
  • FMFn = 119
  • Healthy controlsn = 61reference
Outcome
Gut microbiota composition in relation to disease characteristics
Methodological details16 s rRNA gene sequencing, multivariable association with linear models (MaAslin2), bacterial network analysis
  • 16 s rRNA gene sequencing
  • Multivariable association with linear models (MaAslin2)
  • Bacterial network analysis

Main finding

As reported in the abstract

Gut microbiota composition
  • FMF patients differ from controls in having increased pro-inflammatory bacteria, such as the Enterobacter, Klebsiella and Ruminococcus gnavus group
  • Disease characteristics and colchicine resistance correlated with homozygous mutations and were associated with specific microbiota alteration
  • Colchicine treatment associated with expansion of anti-inflammatory taxa such as Faecalibacterium and Roseburia
  • FMF severity associated with expansion of the Ruminococcus gnavus group and Paracoccus
  • Colchicine-resistant patients: altered bacterial network structure, with decreased intertaxa connectivity
  • Adjusted on age, sex, genotype, AA amyloidosis, hepatopathy, colchicine intake, colchicine resistance, biotherapy, CRP levels, and number of daily faeces

Observational data: associations, not effects.

Original publication

Gut microbiota alterations are associated with phenotype and genotype in familial Mediterranean fever. Rheumatology (Oxford). Published 4 July 2023. doi:10.1093/rheumatology/kead322

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