-derived indole derivatives ameliorate intestinal barrier damage in rat pups with complementary food administration.

The consumption of complementary foods can bring about diarrhea and intestinal barrier dysfunction in infants. In this study, three different strains combined with L-tryptophan (Trp) were administered to rat pups with complementary foods. Complementary food feeding caused inflammatory cell infiltration, crypt structure irregularity and goblet cell reduction in the colon tissues of the rat pups.

-Derived Indole-3-lactic Acid Ameliorates Intestinal Barrier Integrity through the AhR/Nrf2/NF-κB Axis.

Our previous studies have shown that DPUL-S164-derived indole-3-lactic acid (ILA) ameliorates intestinal epithelial cell barrier injury by activating aryl hydrocarbon receptor (AhR) and nuclear factor erythroid 2-related factor 2 (Nrf2) signaling pathways and promoting tight junction protein expression. This study further explored the crucial substances of DPUL-S164 in alleviating intestinal barrier damage in mice through a dextran sodium sulfate-induced ulcerative colitis mouse model. Compared to dead DPUL-S164 (D-S164), live DPUL-S164 (S164) and its tryptophan metabolite, ILA, showed an effective ameliorating effect on the intestinal barrier injury of mice treated by antibiotic cocktail and sodium dextran sulfate, suggesting that the crucial substances of DPUL-S164 ameliorating intestinal barrier injury are its extracellular metabolites.

Indole-3-Lactic Acid, a Tryptophan Metabolite of DPUL-S164, Improved Intestinal Barrier Damage by Activating AhR and Nrf2 Signaling Pathways.

A growing body of evidence suggests that microbial tryptophan metabolites play a crucial role in maintaining intestinal barrier stability and modulating host immunity. Our previous study showed that the ( ) DPUL-S164 intervention in mice with a high tryptophan (Trp) diet promotes indole-3-lactic acid (ILA) production in the mice's intestinal tract and ameliorates dextran sodium sulfate(DSS)-induced intestinal barrier damage in mice. In this study, we used the HT-29 cell monolayer model to evaluate the effect of the DPUL-S164 Trp metabolites (DPUL-S164-TM) on the intestinal barrier.

Changes in Intracellular and Extracellular Metabolites of Mixed Lactobacillus Strains Enhance Inhibition of Pathogenic Bacterial Growth and Lipopolysaccharide-Induced Alleviation of RAW264.7 Cellular Inflammation.

It is important to explore whether there are antagonistic and synergistic effects between different strains of Lactobacillus when developing mixed Lactobacillus strain products. In this study, we investigated the antagonistic and symbiotic effects of co-cultured Lactobacillus strains, as well as their amelioratory effects on lipopolysaccharide (LPS)-induced inflammation and oxidative stress in RAW264.7 cells.

-12 Alleviates Inflammation and Colon Cancer Symptoms in AOM/DSS-Treated Mice through Modulating the Intestinal Microbiome and Metabolome.

In our previous research, Lactiplantibacillus plantarum-12 alleviated inflammation in dextran sodium sulfate (DSS)-induced mice by regulating intestinal microbiota and preventing colon shortening (p < 0.05). The purpose of the present study was to evaluate whether L.

Exopolysaccharide Produced by -12 Alleviates Intestinal Inflammation and Colon Cancer Symptoms by Modulating the Gut Microbiome and Metabolites of C57BL/6 Mice Treated by Azoxymethane/Dextran Sulfate Sodium Salt.

Exopolysaccharide produced by -12 (LPEPS) exhibited the anti-proliferating effect on human colon cancer cell line HT-29 in vitro. The purpose of the study was to determine the alleviating effects of LPEPS on colon cancer development of the C57BL/6 mice treated by azoxymethane/dextran sulfate sodium salt (AOM/DSS). The C57BL/6 mice treated by AOM/DSS were orally administered LPEPS daily for 85 days.