Dairy products—encompassing yogurt, kefir, cheese, and cultured milk beverages—are emerging as versatile, food-based modulators of gut microbiota and host physiology. This review synthesizes mechanistic insights demonstrating how live starter cultures and their fermentation-derived metabolites (short-chain fatty acids, bioactive peptides, and exopolysaccharides) act synergistically to enhance microbial diversity, reinforce epithelial barrier integrity via upregulation of tight-junction proteins, and modulate immune signaling. Clinical evidence supports significant improvements in metabolic parameters (fasting glucose, lipid profiles, blood pressure) and reductions in systemic inflammation across metabolic syndrome, hypertension, and IBS cohorts. We highlight critical modulatory factors—including strain specificity, host enterotypes and FUT2 genotype, fermentation parameters, and matrix composition—that govern probiotic engraftment, postbiotic yield, and therapeutic efficacy. Despite promising short-term outcomes, current studies are limited by heterogeneous designs and brief intervention periods, underscoring the need for long-term, adaptive trials and integrative multi-omics to establish durability and causality. Looking forward, precision nutrition frameworks that harness baseline microbiota profiling, host genetics, and data-driven fermentation design will enable bespoke fermented dairy formulations, transforming these traditional foods into next-generation functional matrices for targeted prevention and management of metabolic, inflammatory, and neuroimmune disorders.

Some strains of lactobacilli can exert beneficial effects on a host when ingested in an adequate dose, such as immunoregulation and anti-inflammatory activities. In this study, the survival abilities under simulated gastrointestinal conditions, adhesion abilities on HT-29 cell monolayers, and hemolytic activities of four Lactobacillus plantarum strains were assessed. Among the four strains, L. plantarum-12 showed the higher survival rate under simulated gastrointestinal conditions and adhesion index on the HT-29 cell monolayers, exhibited γ-haemolytic activity and had no biological amine producing ability. L. plantarum-12 was administered to dextran sodium sulfate (DSS)-induced ulcerative colitis (UC) Balb/c mice by oral gavage for 10 days. It was observed that the UC Balb/c mice showed symptoms of colonic atrophy, intestinal histopathological change, gut microbial disturbance, and pro-inflammatory cytokine expression. L. plantarum-12 administration remarkably attenuated DSS-induced UC in mice. L. plantarum-12 administration could restore gut microbiota by increasing beneficial bacteria such as Lactobacillus and decreasing intestinal pathogenic bacteria like Proteobacteria. L. plantarum-12 administration could improve immunity via activating the janus kinase-signal transducer and the activator of the transcription (JAK-STAT) pathway and up-regulating adenosine deaminase (ADA) and interferon-induced protein with tetratricopeptide repeats 1 protein (IFIT1), and enforce the intestinal barrier function by up-regulating mucin 2 (MUC2) protein expression. In conclusion, L. plantarum-12 could attenuate DSS-induced UC in Balb/c mice by ameliorating intestinal inflammation, and restoring the disturbed gut microbiota. L. plantarum-12 could be used as promising probiotics to ameliorate colitis.

In our previous studies, Lactobacillus plantarum Y44 showed antioxidant activity and favorable gastric and intestinal transit tolerance. The purpose of this study is to determine whether L. plantarum Y44 could ameliorate intestinal inflammation and lipid metabolism disorder in obese mice fed with a high-fat diet. L. plantarum Y44 was administered by gavage to the mice fed with a high-fat diet for 12 weeks. The mice fed with a high fat diet only showed sustainably elevated body weight, liver lipid metabolism disorder, intestinal inflammation and a lower short chain fatty acid content in feces. Oral administration of L. plantarum Y44 regulated lipid metabolism disorder by inhibiting the expression of fatty acid synthase (FAS) and acetyl-CoA carboxylase (ACC) in the liver of obese mice, reducing the contents of total cholesterol (TC), triacylglycerols (TG), low density lipoprotein cholesterol (LDL-c), alanine aminotransferase (ALT), and aspartate transaminase (AST) and increasing the content of high-density lipoprotein cholesterol (HDL-c) in the serum of obese mice. Oral administration of L. plantarum Y44 up-regulated the expression of colon tight junction protein such as claudin-1 and occludin, down-regulated p38 and phospho-p38 levels and reduced serum interleukin-8 (IL-8) and tumor necrosis factor-α (TNF-α). Oral administration of L. plantarum Y44 increased Muribaculaceae, Rikenellaceae, and Lactobacillaceae levels, reduced the Firmicutes/Bacteroidetes ratio, and Desulfovibrionaceae and Proteobacteria levels in obese mice. Oral administration of L. plantarum Y44 also enhanced the contents of propionic acid, butyric acid, butanoicacid-3-methyl, pentanoic acid and acetic acid in the feces of the obese mice. Correlation analysis of Spearman revealed a significant correlation between changes in intestinal microflora and obesity-related symptoms. L. plantarum Y44 ameliorated intestinal inflammation and lipid metabolism disorders by modulating gut microbiota.

Probiotics have been proved to ameliorate the symptoms of the host induced by oxidative stress. In this study, the protective effects of Lactobacillus plantarum Y44 on Balb/C mice injured by D-galactose (D-gal)-injection were examined. Six weeks of continuous subcutaneous D-gal injection caused liver and colon injury of the Balb/C mice. L. plantarum Y44 administration significantly reversed the injury by modulating hepatic protein expressions related to the Nrf-2/Keap-1 pathway, and enhancing expressions of colonic tight junction proteins. L. plantarum Y44 administration restored the D-gal injection-induced gut microbiota imbalance by manipulating the ratio of Firmicutes/Bacteroidetes (F/B) and Proteobacteria relative abundance at the phylum level, and manipulating relative abundances of Lactobacillaceae, Muribaculaceae, Ruminococcaceae, Desulfovibrionaceae, and Prevotellaceae at the family level. Moreover, the D-gal injection-induced glycerophospholipid metabolism disorder was ameliorated, evidenced by the decline of phosphatidyl ethanolamine (PE), phosphatidylcholine (PC), phosphatidyl serine (PS), and lysophosphatidyl choline (LysoPC) levels in the serum of the mice after the L. plantarum Y44 administration. Spearman correlation analysis revealed a significant correlation between changes in gut microbiota composition, glycerophospholipid levels, and oxidative stress-related indicators. In summary, L. plantarum Y44 administration ameliorated D-gal injection-induced oxidative stress in Balb/C mice by manipulating gut microbiota and intestinal barrier function, and further influenced the glycerophospholipid metabolism and hepatic Nrf-2/Keap-1 pathway-related protein expressions.

In our previous studies, Lactobacillus plantarum Y44 showed antioxidant activity and favorable gastric and intestinal transit tolerance. In the current study, we investigated the physiological function of L. plantarum Y44 based on an analysis of its genotype and phenotype. The complete genome of L. plantarum Y44 contained a single circular chromosome of 3,255,555 bp, with a GC content of 44.6%, and a single circular plasmid of 51,167 bp, with a GC content of 38.8%. The L. plantarum Y44 genome contained 3,293 genes including 3,112 protein coding sequences, 16 rRNAs, 66 tRNAs, 4 small (s)RNAs, and 95 pseudo genes. Lactobacillus plantarum Y44 could metabolize 24 different carbohydrate sources. Nineteen complete phosphoenolpyruvate-dependent sugar phosphotransferase system complex genes and intact Embden-Meyerhof-Parnas pathway and hexose monophosphate pathway enzyme genes, as well as abundant carbohydrate active enzyme genes, were identified in the L. plantarum Y44 genome. We also identified genes related to the biosynthesis of exopolysaccharide and surface proteins. Surface proteins played an important role in the L. plantarum Y44 adhesion to HT-29 cell monolayers, as evidenced by the removal of cell surface proteins leading to decreased adhesion capacity. The L. plantarum Y44 genome contained genes encoding chaperones, intracellular proteases, and 2-component systems, which were associated with the general stress response. Genes encoding bile salt hydrolase, F0F1-ATPase, Na+/H+-antiporter, H+/Cl- exchange transporter, cyclopropane-fatty acyl-phospholipid synthase, and alkaline shock protein were identified in the L. plantarum Y44 genome, which might explain the strain's favorable gastric and intestinal transit tolerance. Some genes associated with encoding the NADH system, glutathione system, and thioredoxin system were predicted via in silico analysis and might account for the strain's ability to scavenge reactive oxygen species. Lactobacillus plantarum Y44 was susceptive to 7 antibiotics and did not produce biogenic amines, likely due to the absence of acquired antibiotic resistance genes and amino acid decarboxylase genes. The phenotype profile of L. plantarum Y44 was associated with its genetic characteristics, indicating that strains with certain physiological functions can be screened by analyzing their phenotypic and genotypic characteristics. Lactobacillus plantarum Y44 has the potential to be used as a starter culture in fermented dairy products.

In this study, the hepatoprotective effect of alkali extract (NE) of water bamboo shoot (WBS) against acute alcoholic liver injury (ALI) in mice was evaluated, and its underlying mechanisms were explored. Animal experiment demonstrated that NE exhibited hepatoprotective effect on alcoholic intake‐induced ALI via significantly enhancing the hepatic activities of alcohol dehydrogenase (ADH), acetaldehyde dehydrogenase (ALDH), superoxide dismutase (SOD), glutathione peroxidase (GSH‐Px), and catalase (CAT), whereas significantly attenuated hepatic levels of malondialdehyde (MDA), interleukin‐1β (IL‐1β), interleukin‐6 (IL‐6), and tumor necrosis factor‐α (TNF‐α). The potential molecular mechanism and bioactive compounds of NE against ALI were explored by bioinformatics analysis and isosinensetin was found to be the major bioactive compounds in NE against ALI. The western blot analysis showed that NE inhibited phosphorylation of p65 and IκBα to suppress the NF‐κB pathway. Overall our result indicated that WBS possesses potential hepatoprotective effects against ALI.