Protective Mechanism of Eurotium amstelodami from Fuzhuan Brick Tea against Colitis and Gut-Derived Liver Injury Induced by Dextran Sulfate Sodium in C57BL/6 Mice

Abstract

The study explored the potential protective impact of the probiotic fungus Eurotium amstelodami in Fuzhuan brick tea on ulcerative colitis, along with the underlying mechanism. A spore suspension of E. amstelodami was administered to C57BL/6 mice to alleviate DSS-induced colitis. The findings indicated that administering E. amstelodami evidently enhanced the ultrastructure of colonic epithelium, showing characteristics such as enhanced TJ length, reduced microvilli damage, and enlarged intercellular space. After HLL supplementation, the activation of the liver inflammation pathway, including TLR4/NF-kB and NLRP3 inflammasome caused by DSS, was significantly suppressed, and bile acid metabolism, linking liver and gut, was enhanced, manifested by restoration of bile acid receptor (FXR, TGR5) level. The dysbiosis of the gut microbes in colitis mice was also restored by HLL intervention, characterized by the enrichment of beneficial bacteria (Lactobacillus, Bifidobacterium, Akkermansia, and Faecalibaculum) and fungi (Aspergillus, Trichoderma, Wallemia, Eurotium, and Cladosporium), which was closely associated with lipid metabolism and amino acid metabolism, and was negatively correlated with inflammatory gene expression. Hence, the recovery of gut microbial community structure, implicated deeply in the inflammatory index and metabolites profile, might play a crucial role in the therapeutic mechanism of HLL on colitis.

Oyster Peptides Ameliorate Dextran Sulfate Sodium-Induced Ulcerative Colitis via Modulating the Gut Microbiota and Inhibiting the TLR4/NF-κB Pathway

“…Imbalances in gut microbes usually lead to an increase in harmful bacteria and a decrease in beneficial bacteria [ 31 ]. The TLR4/NF-κB signaling pathway plays a critical role in the progression of colitis in mice and can mediate biological processes such as immunity and inflammation [ 56 ]. LPS produced by harmful bacteria can bind TLR4 on the cell membrane surface and promote the expression of inflammatory factors by activating the NF-κB signaling pathway [ 57 ].…”