In recent years, Blautia has attracted attention for its role in ameliorating host diseases. In particular, Blautia producta DSM 2950 has been considered a potential probiotic due to its ability to mitigate inflammation in poly(I:C) induced HT-29 cells. Thus, to promote the development of indigenous intestinal microorganisms with potential probiotic function, we conducted a comprehensive experimental analysis of DSM 2950 to determine its safety. This comprised a study of its potential virulence genes, antibiotic resistance genes, genomic islands, antibiotic resistance, and hemolytic activity and a 14-day test of its acute oral toxicity in mice. The results indicated no toxin-related virulence genes in the DSM 2950 genome. Most of the genomic islands in DSM 2950 were related to metabolism, rather than virulence expression. DSM 2950 was sensitive to most of the tested antibiotics but was tolerant of treatment with kanamycin, neomycin, clindamycin, or ciprofloxacin, probably because it possessed the corresponding antibiotic resistance genes. Oral acute toxicity tests indicated that the consumption of DSM 2950 does not cause toxic side effects in mice. Overall, the safety profile of DSM 2950 confirmed that it could be a candidate probiotic for use in food and pharmaceutical preparations.

Background: Colonic and serum inosine are significantly reduced in patients with inflammatory bowel disease (IBD). Methods: This study aimed to explore whether microbiome-derived inosine alleviates colitis and its underlying mechanisms. Results: An inosine intervention effectively improved the clinical signs in colitis mice, suppressed inflammatory cytokines (tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), and IL-1β) by regulating the nuclear factor-kappa B (NF-κB) pathway, and elevated the activities of anti-oxidative enzymes (including superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px)) by regulating the nuclear factor erythroid-2 related factor 2 (Nrf2) pathway. Additionally, the inosine intervention significantly elevated the expression of tight junction proteins (ZO-1, occudin, and claudin-1) in mice with colitis. High-throughput sequencing revealed that the inosine intervention also prevented gut microbiota disorder by increasing the abundance of beneficial bacteria (Lachnospiraceae NK4A136 group, Romboutsia, Marvinbryantia, Clostridium sensu stricto 1, and Bifidobacterium) and reducing the abundance of harmful bacteria (Pseudomonas, Acinetobacter, and Tyzzerella) in mice with colitis. Conclusions: Inosine played a significant role in mitigating colitis-related intestinal barrier injury and could potentially be used for therapy in clinical practice.

Background: Lactobacillus paracasei CCFM1223, a probiotic previously isolated from the healthy people’s intestine, exerts the beneficial influence of preventing the development of inflammation. Methods: The aim of this research was to explore the beneficial effects of L. paracasei CCFM1223 to prevent lipopolysaccharide (LPS)-induced acute liver injury (ALI) and elaborate on its hepatoprotective mechanisms. Results: L. paracasei CCFM1223 pretreatment remarkably decreased the activities of serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) in mice with LPS treatment and remarkably recovered LPS-induced the changes in inflammatory cytokines (tumor necrosis factor-α (TNF-α), transforming growth factor-β (TGF-β), interleukin (IL)-1β, IL-6, IL-17, IL-10, and LPS) and antioxidative enzymes activities (total antioxidant capacity (T-AOC), superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and catalase (CAT)). Metagenomic analysis showed that L. paracasei CCFM1223 pretreatment remarkably increased the relative abundance of Catabacter compared with the LPS group but remarkably reduced the relative abundance of [Eubacterium] xylanophilumgroup, ASF356, LachnospiraceaeNK4A136group, and Lachnoclostridium, which is closely associated with the inflammation cytokines and antioxidative enzymes. Furthermore, L. paracasei CCFM1223 pretreatment remarkably increased the colonic, serum, and hepatic IL-22 levels in ALI mice. In addition, L. paracasei CCFM1223 pretreatment remarkably down-regulated the hepatic Tlr4 and Nf-kβ transcriptions and significantly up-regulated the hepatic Tlr9, Tak1, Iκ-Bα, and Nrf2 transcriptions in ALI mice. Conclusions: L. paracasei CCFM1223 has a hepatoprotective function in ameliorating LPS-induced ALI by regulating the “gut–liver” axis.

Lacticaseibacillus rhamnosus is a strain predominantly used for juice production because of its excellent fermentation characteristics and strong acid production capacity. However, the influence of L. rhamnosus on the quality of mango juice has not yet been determined. Therefore, the effects of L. rhamnosus FJG1530 on the physicochemical properties, physiological activity, and volatile and non-volatile compounds of mango juice were extensively examined in this study. The data showed that L. rhamnosus FJG1530 possessed strong adaptability to mango juice, reducing its total sugar and increasing its total flavonoids. L. rhamnosus FJG1530 fermentation enhanced the ability of mango juice to clear the free radicals ABTS and DPPH, as well as improving the inhibition of lipase and α-glucosidase. In addition, L. rhamnosus FJG1530 treatment improved the volatile compounds in mango juice, especially promoting the formation of acids and alcohols. Simultaneously, metabolomic analysis revealed that 592 non-volatile compounds in mango juice were significantly changed by L. rhamnosus FJG1530 fermentation, with 413 dramatically increased and 179 significantly decreased metabolites. This study demonstrates that the fermentation process using L. rhamnosus FJG1530 was beneficial for ameliorating the quality of mango juice.

Colitis is a global health challenge that severely impairs quality of life, necessitating effective dietary interventions. This study investigated the protective effects of Ganoderma lucidum triterpenoids (GLTs) on pathological symptoms, inflammatory responses, and gut microbiota dysbiosis in a dextran sulfate sodium (DSS)-induced murine model. Our results demonstrated that GLT intervention significantly attenuated the disease activity index (DAI), prevented colon shortening, and fortified gut barrier integrity through upregulating the transcription of tight junction proteins. GLT inhibited the secretion of pro-inflammatory cytokines (TNF-α, IL-1β, and IL-6) and bolstered antioxidant defenses (CAT) by controlling the TLR4/NF-κB pathway and upregulating the Nrf2 pathway. Furthermore, 16S rRNA sequencing and non-targeted metabolomics revealed that GLT reshaped the gut microbial landscape (enriching Enterorhabdus and Lachnospiraceae NK4A136 group) and reconfigured amino acid metabolism to restore colonic homeostasis. Collectively, these findings highlight the potential of GLT as a functional food ingredient to prevent colitis, potentially linked to the modulation of the microbiota–metabolite–immune interplay, offering a novel nutritional strategy for inflammatory bowel disease management.

As a natural polysaccharide, sulfated fucan from sea cucumber possesses multiple biological activities, but its protective effect on acute liver injury (ALI) is still unclear. The aim of this study was to clarify the protective effects of sulfated fucan from sea cucumber on lipopolysaccharide (LPS)-induced ALI in mice. After administering sulfated fucan from sea cucumber (100 mg kg⁻¹ d⁻¹) to mice via gavage for 14 days, an ALI model was induced by intraperitoneal injection of LPS. The results showed that pretreatment with sulfated fucan from sea cucumber significantly reduced serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), and alkaline phosphatase (ALP) levels, alleviated histopathological liver damage, suppressed the expression of pro-inflammatory factors (tumor necrosis factor (TNF)-α, interleukin (IL)-1β and IL-6), elevated the anti-inflammatory factor level (IL-10), and enhanced the activity of antioxidant enzymes (superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and catalase (CAT)). Additionally, FUC suppressed the toll-like receptor 4 (TLR4)/myeloid differentiation primary response 88 (MyD88)/nuclear factor-kappa B (NF-κB) pathway and activated the nuclear factor erythroid 2-related factor 2 (Nrf2)/heme oxygenase (HO)-1 pathway gene expression. 16S rRNA sequencing indicated that sulfated fucan from sea cucumber mainly increased the proportions of Lachnospiraceae_NK4A136_group and Christensenellaceae_R-7_group. Liver metabolomics analysis revealed that FUC reversed LPS-induced disturbances in purine metabolism, arachidonic acid metabolism, and tryptophan metabolism. This study demonstrates that sulfated fucan from sea cucumber exerts hepatoprotective effects by modulating the “gut–liver axis”, providing a scientific basis for its use as a functional food or dietary supplement in the prevention of ALI.