Lacticaseibacillus rhamnosus LS8 Ameliorates Azoxymethane/Dextran Sulfate Sodium-Induced Colitis-Associated Tumorigenesis in Mice via Regulating Gut Microbiota and Inhibiting Inflammation.

Gut microbiota dysbiosis may promote the process of colorectal cancer (CRC). Lacticaseibacillus rhamnosus LS8 (LRL) is a potential gut microbiota regulating strain because it can produce a novel antimicrobial substance (like cycloalanopine). In addition, this probiotic had an inflammation-ameliorating effect on the dextran sulfate sodium (DSS)-induced colitis mice. However, it is not known whether treatment with this probiotic could ameliorate colitis-associated CRC via regulating gut microbiota. In this study, a CRC mouse model was induced by a single intraperitoneal injection of azoxymethane (AOM, 10 mg/kg) and followed by three 7-day cycles of 2% DSS administration. Results showed that LRL could inhibit tumor formation. Moreover, LRL enhanced the gut barrier by preventing goblet cell loss and promoting the expression of ZO-1, occludin, and claudin-1. Furthermore, LRL ameliorated gut microbiota dysbiosis, which was conducive to the growth of beneficial bacteria (e.g., Faecalibaculum and Akkermansia), and further led to an increase in SCFAs and a decrease in LPS. In addition, LRL alleviated colonic inflammation by inhibiting the overexpression of TLR4/NF-κB, pro-inflammatory cytokines (TNF-α, IL-1ß, IL-6, IL-γ, and IL-17a), and chemokines (Cxcl1, Cxcl2, Cxcl3, Cxcl5, and Cxcl7). In conclusion, LRL could alleviate CRC by regulating gut microbiota and preventing gut barrier damage and inflammation.

Protective Effects of Companilactobacillus crustorum MN047 against Dextran Sulfate Sodium-Induced Ulcerative Colitis: A Fecal Microbiota Transplantation Study.

Gut microbiota dysbiosis could aggravate the development of ulcerative colitis (UC). Companilactobacillus crustorum MN047 (CCMN) is a potential gut microbiota-regulating probiotic that could produce multiple novel bacteriocins. In this study, fecal microbiota transplantation (FMT) was used to verify whether CCMN could alleviate dextran sulfate sodium-induced UC by regulating gut microbiota. Results showed that both CCMN and FMT ameliorated the symptoms of UC, including attenuating the increased disease activity index, shortened colon length, gut barrier damage, and inflammation. Briefly, CCMN and FMT upregulated the expressions of MUCs and tight junctions, downregulated the expressions of proinflammatory cytokines and chemokines, increased fecal short-chain fatty acids, and lowered serum lipopolysaccharides, which were associated with the regulation of gut microbiota (e.g., increased Akkermansia, Blautia, and Ruminococcus levels). These results demonstrated that CCMN could ameliorate UC by modulating gut microbiota and inhibiting the TLR4/NF-κB pathway. Therefore, CCMN could be considered as a potential probiotic supplement for ameliorating UC.