Effects of Latilactobacillus sakei LZ217 on Gastric Mucosal Colonization, Metabolic Interference, and Urease Expression in Helicobacter pylori Infection.

Emerging evidence suggests differential antagonism of lactic acid-producing bacteria (LAB) to Helicobacter pylori, posing challenges to human health and food safety due to unclear mechanisms. This study assessed 21 LAB strains from various sources on H. pylori growth, urease activity, and coaggregation. Composite scoring revealed that Latilactobacillus sakei LZ217, derived from fresh milk, demonstrates strong inhibitory effects on both H. pylori growth and urease activity. L. sakei LZ217 significantly reduced H. pylori adherence of gastric cells in vitro, with inhibition ratios of 47.62%. Furthermore, in vivo results showed that L. sakei LZ217 alleviated H. pylori-induced gastric mucosa damage and inflammation in mice. Metabolomic exploration revealed metabolic perturbations in H. pylori induced by L. sakei LZ217, including reduced amino acid levels (e.g., isoleucine, leucine, glutamate, aspartate, and phenylalanine) and impaired carbohydrate and nucleotide synthesis, contributing to the suppression of ureA (28.30%), ureE (84.88%), and ureF (59.59%) expressions in H. pylori. This study underscores the efficacy of LAB against H. pylori and highlights metabolic pathways as promising targets for future interventions against H. pylori growth and colonization.

Role of folic acid in regulating gut microbiota and short-chain fatty acids based on an in vitro fermentation model.

Folic acid deficiency is common worldwide and is linked to an imbalance in gut microbiota. However, based on model animals used to study the utilization of folic acid by gut microbes, there are challenges of reproducibility and individual differences. In this study, an in vitro fecal slurry culture model of folic acid deficiency was established to investigate the effects of supplementation with 5-methyltetrahydrofolate (MTHF) and non-reduced folic acid (FA) on the modulation of gut microbiota. 16S rRNA sequencing results revealed that both FA (29.7%) and MTHF (27.9%) supplementation significantly reduced the relative abundance of Bacteroidetes compared with control case (34.3%). MTHF supplementation significantly improved the relative abundance of Firmicutes by 4.49%. Notably, compared with the control case, FA and MTHF supplementation promoted an increase in fecal levels of Lactobacillus, Bifidobacterium, and Pediococcus. Short-chain fatty acid (SCFA) analysis showed that folic acid supplementation decreased acetate levels and increased fermentative production of isobutyric acid. The in vitro fecal slurry culture model developed in this study can be utilized as a model of folic acid deficiency in humans to study the gut microbiota and demonstrate that exogenous folic acid affects the composition of the gut microbiota and the level of SCFAs. KEY POINTS: • Establishment of folic acid deficiency in an in vitro culture model. • Folic acid supplementation regulates intestinal microbes and SCFAs. • Connections between microbes and SCFAs after adding folic acid are built.

Metabolism of quercitrin in the colon and its beneficial regulatory effects on gut microbiota.

BACKGROUND: Quercitrin is a dietary flavonoid widely found in plants with various physiological activities. However, whether quercitrin alters gut microbiota in vivo is not well understood. The aim of this study was to investigate metabolism of quercitrin in the colon and its regulation on gut microbiota in mice. RESULTS: Herein, 22 flavonoids related to quercitrin metabolism were identified based on ultra-performance liquid chromatography-electrospray ionization-tandem mass spectrometry (UPLC-ESI-MS/MS). Gas chromatography and 16S rDNA gene sequencing were used to investigate short-chain fatty acid (SCFA) content and diversity of composition of gut microbiota, respectively. The results showed that quercitrin significantly alters the beta-diversity of the gut microbiota, probiotics such as Akkermansia and Lactococcus were significantly increased, and the production of propanoate, isovalerate and hexanoate of the quercitrin group were enhanced significantly. The Spearman's association analysis provided evidence that Gardnerella and Akkermansia have obvious correlations with most of quercitrin metabolites and SCFAs. CONCLUSION: Quercitrin and its metabolites in the colon altered the structure of the mice gut microbiota and increased the content of SCFAs. Our experiments provide valuable insights into quercitrin research and application. © 2024 Society of Chemical Industry.

Lactiplantibacillus plantarum ZJ316-fermented milk ameliorates dextran sulfate sodium-induced chronic colitis by improving the inflammatory response and regulating intestinal microbiota.

The pathogenesis of inflammatory bowel disease may be related to local inflammatory damage and disturbances in intestinal microecology. Probiotic therapy is a safe and effective therapeutic approach. Considering that fermented milk is accepted and enjoyed by many people as a daily dietary intervention strategy, its potential to alleviate dextran sulfate sodium (DSS)-induced chronic colitis in mice needs to be explored. In this study, we evaluated the therapeutic effects of Lactiplantibacillus plantarum ZJ316-fermented milk by establishing a mouse model of DSS-induced chronic colitis. The results showed that the disease severity and colonic lesions of inflammatory bowel disease were effectively alleviated by ingestion of fermented milk. At the same time, the expression of proinflammatory cytokines (TNF-α, IL-1ß, and IL-6) effectively decreased, and the expression of antiinflammatory cytokines (IL-10) increased. Results based on 16S rRNA gene sequencing indicated that the structure and diversity of intestinal microorganisms changed markedly by intake of L. plantarum ZJ316-fermented milk, and fermented milk reduced the abundance of harmful bacteria (Helicobacter) while promoting the growth of beneficial bacteria (Faecalibacterium, Lactiplantibacillus, and Bifidobacterium). Additionally, the levels of short-chain fatty acids (acetic acid, propionic acid, butyric acid, pentanoic acid, and isobutyric acid) were also increased. In conclusion, the intake of L. plantarum ZJ316-fermented milk can alleviate chronic colitis by suppressing the inflammatory response and regulating intestinal microbiota.

Soluble Dietary Fiber from Citrus unshiu Peel Promotes Antioxidant Activity in Oxidative Stress Mice and Regulates Intestinal Microecology.

Aging is characterized by the progressive degeneration of bodily tissues and decline in physiological functions, a process that may be exacerbated by imbalances in intestinal flora. Soluble dietary fiber (PSDF) from Citrus unshiu peel has demonstrated strong free radical scavenging ability to regulate intestinal flora in vitro. However, further evidence is required to ascertain the effectiveness of PSDF in vivo. In our study, 8-week-old mice were artificially aged through subcutaneous injections of a 200 mg/kg/d D-galactose solution for 42 days, followed by a 28-day dietary intervention with varying doses of PSDF, insoluble dietary fiber (PIDF), and vitamin C. After the intervention, we observed a significant mitigation of D-galactose-induced oxidative stress, as evident by weight normalization and reduced oxidative damage. 16S rRNA gene sequencing revealed that PSDF significantly altered the composition of intestinal flora, increasing Firmicutes and reducing Bacteroidota percentages, while also enriching colonic short-chain fatty acids (SCFAs). Spearman correlation analysis further identified a positive correlation between Firmicutes and isovaleric acid, and negative correlations between Muribaculaceae and acetic acid, and between Lachnospiraceae_NK4A136_group and caproic acid. These findings support the potential of Citrus PSDF to alleviate oxidative stress.

Lactobacillus plantarum ZJ316 alleviates ulcerative colitis by inhibiting inflammation and regulating short-chain fatty acid levels and the gut microbiota in a mouse model.

Ulcerative colitis is an inflammatory bowel disease that is mainly related to gut microbiota dysbiosis. Lactobacillus plantarum ZJ316 (ZJ316) has been proved to regulate the gut microbiota in vitro. However, more evidence is needed for the intestinal effects of ZJ316 in vivo. Colitis was induced via dissolved 2.5% DSS in drinking water for 7 days in 8-week-old BALB/c mice, which were then fed with ZJ316 (1 × 108 CFU mL-1) for 35 days. After ZJ316 intervention, the dextran sulfate sodium salt (DSS)-induced colitis symptoms were remarkably alleviated, including recovery of body weight and colon weight and effective inhibition of the expression of pro-inflammatory cytokines. Results based on 16S rRNA gene sequencing indicated that the structure of the gut microbiota in ZJ316 supplementation was markedly altered by upregulating the percentage of Firmicutes while reducing the percentage of Bacteroidetes. Furthermore, the colon contained more short-chain fatty acids (SCFAs) and butyrate-producing genera, such as Faecalibacterium, Agathobacter, and Roseburia. Spearman correlation analysis indicated that SCFAs, especially butyric acid, were positively associated with Faecalibacterium and Agathobacter. Our study suggested that ZJ316 could be used to relieve ulcerative colitis (UC) as dietary therapeutics.

Lactiplantibacillus plantarum ZJ316 Reduces Helicobacter pylori Adhesion and Inflammation by Inhibiting the Expression of Adhesin and Urease Genes.

SCOPE: The present study aims to investigate the anti-Helicobacter pylori (H. pylori) effects of Lactiplantibacillus plantarum ZJ316 (L. plantarum ZJ316) both in vitro and in vivo. METHODS AND RESULTS: This study finds that L. plantarum ZJ316 effectively suppresses H. pylori adhesion in inhibition (Pre-ZJ316), competition (Co-ZJ316), and displacement (Post-ZJ316) assays, and Pre-ZJ316 displaying the most potent inhibitory effect with an impressive inhibition ratio of 70.14%. Upon anti-adhesion, L. plantarum ZJ316 significantly downregulates the expression of H. pylori virulence genes, including ureA, ureB, flaA, and sabA, with inhibition ratios of 46.83%, 24.02%, 21.42%, and 62.38% at 2 h, respectively. In addition, L. plantarum ZJ316 is observed to reduce the level of interleukin 8 (IL-8) and improve cell viability in infected AGS cells. Furthermore, in vivo studies show that supplementation with L. plantarum ZJ316 effectively hinders H. pylori colonization and significantly suppresses the infiltration of immune cells and IL-8 production with H. pylori infection, protecting host from inflammatory damage. CONCLUSION: L. plantarum ZJ316 exhibits excellent adhesion inhibition on H. pylori, and may be used as a probiotic candidate in the prevention or adjuvant therapy of gastric disease caused by H. pylori.

Free fatty acids responsible for characteristic aroma in various sauced-ducks.

To investigate the effects of various duck sources on the lipid oxidation and aroma flavor of sauced-ducks, Mallard (ML), Sheldrake (SD), Muscovy (MC), and Cherry-Valley (CV) ducks were used in sauced-duck processing. The results showed significantly different thiobarbituric acid reactive substances (TBARS) values of the four samples (SD > CV > ML > MC, p < 0.05), while the contents of unsaturated fatty acids (UFAs) were ML > SD/CV > MC (p < 0.05). Altogether, 105 volatile flavor compounds were detected in sauced-ducks, including acids, alcohols, aldehydes, ketones, esters, hydrocarbons, furans, nitrogen compounds, and others. The volatile compounds were observed differentially composed in the four products, and nineteen potential characteristic biomarkers were explored. The correlation analysis indicated that the characteristic aroma flavor of sauced-ducks were significantly associated with specific free fatty acids. These information are useful for learning aroma formation and meat selection and identification in duck products.

Volatile flavor changes responding to heat stress-induced lipid oxidation in duck meat.

The effects of heat stress on lipid oxidation and volatile compounds in duck meat were investigated. To simulate heat stress on ducks, room-temperature was controlled at 25°C, except that a raised temperature of 32°C for 8 hr each day was conducted. After stress for 1 and 3 weeks, respectively, the birds were euthanized and the breast meat was separated to evaluate the changes of lipid oxidation and volatile flavor compounds. Results showed that heat stress significantly increased the lipoxygenase activity and thiobarbituric acid reactive substances, and reduced the contents of free unsaturated fatty acids in duck meat. A total of 85 volatile flavor compounds were detected by gas chromatography-mass spectrometry. Interestingly, when exposed to heat stress, the volatiles generation in raw duck meat was promoted, which was then inhibited after cooking. These data reveal meat oxidative changes and flavor loss caused by heat stress and provide useful information for potential labels and meat flavor preservation against the negative effects of heat stress.

Proteomic responses to oxidative damage in meat from ducks exposed to heat stress.

Heat stress causes oxidative damage and quality reduction in poultry. Here, a tandem mass tag proteomic approach was applied to investigate the proteomic differences in duck meat from birds exposed to heat stress. Altogether 212 differential proteins were identified, including 178 down-regulated and 34 up-regulated proteins, compared to the control. Malondialdehyde and carbonyl content and cooking loss of the chest muscle significantly increased under heat stress. The proteomic analysis indicated that heat stress suppressed mitochondrial functions and respiratory chains, which might be responsible for the higher oxidation level. The results also revealed potential protective proteins involved in the defensive mechanisms against heat stress in duck muscles, such as sarcoplasmic/endoplasmic reticulum calcium ATPases, Mn-superoxide dismutase, heat shock protein family B member 7, methyltransferase like 21C, myosin-binding protein C, and carbonic anhydrase 3. These results provide potential targets for the research and identification of oxidative meat products due to heat stress.