Foods rich in ellagic tannins are first hydrolyzed into ellagic acid in the stomach and small intestine, and then converted into urolithins with high bioavailability by the intestinal flora. Urolithin has beneficially biological effects, it can induce adipocyte browning, improve cholesterol metabolism, inhibit graft tumor growth, relieve inflammation, and downregulate neuronal amyloid protein formation via the β3-AR/PKA/p38MAPK, ERK/AMPKα/SREBP1, PI3K/AKT/mTOR signaling pathways, and TLR4, AHR receptors. But differences have been reported in urolithin production capacity among different individuals. Thus, it is of great significance to explore the biological functions of urolithin, screen the strains responsible for biotransformation of urolithin, and explore the corresponding functional genes. Tannin acyl hydrolase can hydrolyze tannins into ellagic acid, and the genera Gordonibacter and Ellagibacter can metabolize ellagic acid into urolithins. Therefore, application of "single bacterium", "single bacterium + enzyme", and "microflora" can achieve biotransformation of urolithin A. In this review, the source and metabolic pathway of ellagic tannins, and the mechanisms of the biological function of a metabolite, urolithin A, are discussed. The current strategies of biotransformation to obtain urolithin A are expounded to provide ideas for further studies on the relationship between urolithin and human health.

Colitis has become a major health concern worldwide. The objective of the present study was to determine the probiotic influence of different strains of B. pseudolongum (Bp7 and Bp8) on alleviating colitis and to explore its possible potential mechanisms. Our results displayed that Bp7 and Bp8 intervention effectively reduced dextran sodium sulfate (DSS)-caused body weight loss and the release of several pro-inflammatory factors (interleukin (IL)-6, IL-1β, and tumor necrosis factor-α (TNF-α)) and increased the activities of antioxidant enzymes (T-AOC, SOD, and GSH) and the concentrations of tight junction proteins (occludin, claudin-1, and ZO-1). Moreover, Bp7 and Bp8 intervention drastically down-regulated the expression of colonic MyD88, NF-κB, iNOS and COX2 and drastically elevated the expression of colonic STAT3, Nrf2, and PPARγ. Gas chromatography-mass spectrometry results revealed that the cecal levels of isobutyric, butyric, and isovaleric acids were drastically increased in colitis mice intervened with Bp7 and Bp8. Moreover, 16S rRNA sequencing revealed that Bp7 and Bp8 intervention modulated the intestinal microbiota structure, particularly by enhancing the proportion of Eubacterium coprostanoligenes group, Marvinbryantia, Enterorhabdus, Faecalibaculum, Coriobacteriaceae UCG 002, Alistipes, and Bifidobacterium, which are relevant to the levels of cecal isobutyric acid, butyric acid, isovaleric acid, and inflammatory cytokines. Collectively, these findings suggest that Bp7 and Bp8 intervention alleviates the intestinal barrier function, possibly by blocking the secretion of proinflammatory cytokines, maintaining the intestinal physical barrier integrity, activating the PPARγ/STAT3 pathway, and modulating intestinal microbiota composition. Our study also suggested that B. pseudolongum is a promising probiotic for colitis treatment.

Epigallocatechin gallate (EGCG), a typical flavone-3-ol polyphenol containing eight free hydroxyl groups, is associated with a variety of bioactivities, such as antioxidant, anti-inflammatory, anti-cancer, and antibacterial activities. However, the poor bioavailability of EGCG restricts its use. In this review, we discuss the processes involved in the absorption and metabolism of EGCG, with a focus on its metabolic interactions with the gut microbiota. Next, we summarize the bioactivities of some key metabolites, describe the biotransformation of EGCG by different microorganisms, and discuss its catabolism by specific bacteria. A deeper understanding of the absorption, metabolism, and biotransformation of EGCG may enable its disease-preventive and therapeutic properties to be better utilized. This review provides a theoretical basis for further development and utilization of EGCG and its metabolites for improving the gut microbiota and physiological health.

Blautia has attracted attention because of its potential efficacy in ameliorating host energy metabolism and inflammation. This study aims to investigate the influences of Blautia producta D4 on colitis induced by dextran sulfate sodium (DSS) and to reveal the underlying mechanisms. Results showed that B. producta D4 intervention significantly relieved body weight loss, and suppressed the elevation of pro-inflammatory cytokines [including interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), and interleukin-1β (IL-1β)] and excessive oxidative stress [myeloperoxidease (MPO) activity, superoxide dismutase (SOD) activity, glutathione peroxidase (GSH-Px) activity, and malondialdehyde (MDA) level] in colitis mice. Moreover, the concentrations of tight junction proteins (occludin, claudin-1, and ZO-1) related to the intestinal barrier were obviously elevated, and colitis-related TLR4/NF-κB pathway activation was remarkably inhibited after B. producta D4 intervention. The intestinal microbial disorder was evidently ameliorated by increasing the relative abundance of Clostridium sensu stricto 1, Bifidobacterium, GCA-900066225, Enterorhabdus, and reducing the relative abundance of Lachnospiraceae NK4A136 group. In conclusion, oral administration of B. producta D4 could ameliorate DSS-induced colitis by suppressing inflammatory responses, maintaining the intestinal barrier, inhibiting TLR4/ NF-κB pathway, and regulating intestinal microbiota balance. These results are conducive to accelerate the development of B. producta D4 as a functional probiotic for colitis.