Metabolites from specific intestinal bacteria in vivo fermenting Lycium barbarum polysaccharide improve collagenous arthritis in rats.

Rheumatoid arthritis (RA) is an autoimmune disease affected patients' quality of life severely. Our previous study found Lycium barbarum polysaccharide (LBP) alleviated RA, but it remains unknown whether gut microbiota is necessary for the alleviation. Here, RA models were established in rats with microbiota and rats treated by antibiotic cocktail, and LBP was applied for the intervention on rats. The biochemical test, 16S rDNA sequencing and metabolome analysis were applied to analyze the effects of LBP on gut microbiota, their metabolites and hosts. Results showed the LBP intervention improved RA by inhibiting pro-inflammatory cytokines IL-1α, IL-1ß, TNF-α and IL-6 only in rats with microbiota, but not in pseudo-germ-free rats. The abundance of specific bacteria, including Romboutsia, Lactobacillus, Turicibacter, Clostridium_sensu_stricto_1, Faecalibacterium and Adlercreutzia, and several metabolites, including O-desmethylangolensin, 3-hydroxydodecanedioic acid, N-formyl-L-methionine, suberic acid, (S)-oleuropeic acid, prolyl-histidine, 13,14-dihydro PGF-1a, (R)-pelletierine and short-chain fatty acids increased only in RA rats with microbiota after the intervention. Our results suggest that intestinal bacteria are necessary for LBP alleviating RA alleviation. The fermentation metabolite acts on the host instead of LBP itself, which may be the reason for the improvement of RA.

Ganoderma lucidum polysaccharide improves rat DSS-induced colitis by altering cecal microbiota and gene expression of colonic epithelial cells.

BACKGROUND: The effects of ß-glucan on colitis mice are contradictory in previous reports. As a result, it is still unclear whether there is an anti-colitis effect in Ganoderma lucidum polysaccharide (GLP), which is mainly composed of ß-glucan. Moreover, the association between GLP function and gut microbiota remains to be elucidated. OBJECTIVE: This study aimed to investigate whether GLP consumption improved rat dextran sodium sulfate (DSS)-induced colitis by regulating gut microbiota and altering colonic epithelial expression. DESIGN: The disease activity index (DAI) scores and the cecal short chain fatty acid (SCFA) levels of DSS-induced colitis rats fed with a GLP diet (Group GLP, n = 6) and a control diet (Group Con, n = 6) were investigated and analyzed. Moreover, the profiles of gut microbiota and colonic epithelial expression were analyzed using metagenomics and transcriptomics. RESULTS: GLP consumption significantly lowered animal DAI scores by producing more SCFAs by increasing SCFA-producing bacteria such as Ruminococcus_1 and reducing pathogens such as Escherichia-Shigella in both the small intestine and cecum of rat. Moreover, GLP consumption regulated 11 genes, including six upregulated (Ccl5, Cd3e, Cd8a, Il21r, Lck, and Trbv) and five downregulated (Ccl3, Gro, Il11, Mhc2, and Ptgs) genes enriched in six inflammation-related Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways, resulting in enhancement of immunity and reduction of inflammatory response and colonic cancer risk. CONCLUSIONS: GLP consumption alleviated DSS-induced colitis and may have potential for ulcerative colitis relief.