ArticleBrain and behavior2025
Amelioration of Central Nervous System Autoimmunity Through FFAR2 Agonism Is Associated With Changes in Gut Microbiota.
Article in Brain and behavior, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
4 citing papers in PubMed.
- FFAR2 activation induces IL-22-dependent intestinal immune responses to suppress CNS autoimmunity.EMBO molecular medicine · 2026Article
- Article
- Gut microbiota-immune crosstalk in osteoarthritis: pathogenic mechanisms and emerging therapeutic opportunities.Frontiers in microbiology · 2026Review
- Mendelian Randomization Unlocks Stroke Therapeutics: Dioscin Inhibits CD27-Driven Neuroinflammation via Gut Microbiota Modulation.Molecular neurobiology · 2025Article
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Authors and funding
8 authors.
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Abstract
purposeThe intestinal immune compartment is increasingly recognized as an important player in central nervous system (CNS) autoimmunity. We have recently reported that oral administration of the free fatty acid receptor 2 (FFAR2) agonist Cpd1 in the inductive phase of experimental autoimmune encephalomyelitis (EAE) in rats ameliorates the disease by stimulating the regulatory immune response in the intestine.
methodHere, the effects of Cpd1 on the gut microbiota and short-chain fatty acid (SCFA) composition were investigated in the same experimental system. FINDING: Increased levels of the phylum Proteobacteria, the class Gammaproteobacteria, the orders Burkholderiales and Erysipelotrichales, the families Sutterellaceae and Erysipelotrichaceae, and the genera Parasutterella and Faecalibaculum were observed in agonist-treated rats. The genera Allobaculum and Ileibacterium were only detected in the agonist-treated group. The treatment led to changes in the functional profile of the gut microbiota both in the KEGG orthologous pathways and in the clusters of orthologous genes. In addition, an altered profile of intestinal SCFA content was observed in the agonist-treated group.
conclusionThe effects of Cpd1 on the gut microbiota and SCFA composition are relevant to the observed treatment benefit of FFAR2 agonism in the EAE model during the inductive phase of the disease.
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