ArticleFrontiers in cellular and infection microbiology2013
Management of familial Mediterranean fever by colchicine does not normalize the altered profile of microbial long chain fatty acids in the human metabolome.
Article in Frontiers in cellular and infection microbiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 12 citations in OpenAlex.
- Familial Mediterranean Fever and the Gut Microbiota: A Dual Perspective Review of Current Evidence.Mediterranean journal of rheumatology · 2026Review
- Gut microbiota alliance to shape sceneries of familial Mediterranean fever: a scoping review detailing difference between children and adults.Frontiers in immunology · 2026Article
- Gut Microbiota between Environment and Genetic Background in Familial Mediterranean Fever (FMF).Genes · 2020Review
- Bile acid analogues are activators of pyrin inflammasome.The Journal of biological chemistry · 2019Article
- Analysis of the gut microbiome and plasma short-chain fatty acid profiles in a spontaneous mouse model of metabolic syndrome.Scientific reports · 2017Article
- Bifidobacteria Abundance-Featured Gut Microbiota Compositional Change in Patients with Behcet's Disease.PloS one · 2016Article
- Systemic Concentrations of Short Chain Fatty Acids Are Elevated in Salmonellosis and Exacerbation of Familial Mediterranean Fever.Frontiers in microbiology · 2016Article
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Authors and funding
12 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In our previous works we established that in an autoinflammatory condition, familial Mediterranean fever (FMF), the gut microbial diversity is specifically restructured, which also results in the altered profiles of microbial long chain fatty acids (LCFAs) present in the systemic metabolome. The mainstream management of the disease is based on oral administration of colchicine to suppress clinical signs and extend remission periods and our aim was to determine whether this therapy normalizes the microbial LCFA profiles in the metabolome as well. Unexpectedly, the treatment does not normalize these profiles. Moreover, it results in the formation of new distinct microbial LCFA clusters, which are well separated from the corresponding values in healthy controls and FMF patients without the therapy. We hypothesize that the therapy alters the proinflammatory network specific for the disease, with the concomitant changes in gut microbiota and the corresponding microbial LCFAs in the metabolome.
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