octadecadienoic-acid has been researched along with Arthritis--Rheumatoid* in 2 studies
2 other study(ies) available for octadecadienoic-acid and Arthritis--Rheumatoid
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Analysis of gut microbiota and metabolites in patients with rheumatoid arthritis and identification of potential biomarkers.
Rheumatoid arthritis (RA) is an autoimmune disease described by joint destruction, synovitis and pannus formation. The gut microbiota acts as an environmental factor that plays an important role in RA, but little research regarding the etiopathogenic mechanisms of the microbiome in RA has been carried out. We used an integrated approach of 16S rRNA gene sequencing and ultrahigh-performance liquid chromatography-mass spectrometry-based metabolomics to analyze the structure and diversity of the intestinal flora and metabolites of the gut microbiota in RA patients compared with healthy subjects. In this study, α-diversity analysis of the gut microbiota showed that there was no significant difference between the healthy control (HC) and RA groups. However, β-diversity analysis showed that there was a significant difference between the two groups. Further analysis of alteration of the gut microbiota revealed that at the phylum level, the relative abundance of p_Bacteroidetes was significantly decreased in the RA group, while that of Verrucomicrobia and Proteobacteria was significantly increased in the RA group. At the genus level, Bacteroides, Faecalibacterium and some probiotics were decreased in the RA group, while 97 genera, including Topics: Adult; Arthritis, Rheumatoid; Biomarkers; DNA, Bacterial; Fatty Acids; Fatty Acids, Unsaturated; Gastrointestinal Microbiome; Humans; Metabolome; Middle Aged; RNA, Ribosomal, 16S | 2021 |
The anti-inflammatory effect of the gut lactic acid bacteria-generated metabolite 10-oxo-cis-6,trans-11-octadecadienoic acid on monocytes.
We evaluated the effect of gut bacterial metabolites of polyunsaturated fatty acids on inflammation and found that 10-oxo-cis-6,trans-11-octadecadienoic acid (γKetoC) strikingly suppressed LPS-induced IL-6 release from bone marrow-derived macrophages (BMMs), which was accompanied by reduced mRNA expression of Il6, TNF, and Il1b. γKetoC decreased the cAMP concentration in BMMs, suggesting that γKetoC stimulated G protein-coupled receptors. A Gq agonist significantly suppressed LPS-induced IL-6 expression in BMMs, whereas a Gi inhibitor partially abrogated γKetoC-mediated IL-6 suppression. Cytosolic Ca Topics: Animals; Arthritis, Rheumatoid; Cell Line; Cells, Cultured; Cytokines; Fatty Acids, Unsaturated; Female; Gastrointestinal Microbiome; Humans; Inflammation; Lactobacillales; Macrophages; Mice; Mice, Inbred C57BL; Monocytes; Protective Factors; RAW 264.7 Cells | 2020 |