Preventive and therapeutic effect of Lactobacillus paracasei ZFM54 on Helicobacter pylori-induced gastritis by ameliorating inflammation and restoring gastric microbiota in mice model.

Helicobacter pylori is the most prevalent pathogen causing chronic gastritis, gastroduodenal ulcers, and gastric tumors and is asymptomatically present in 50% of the world's population. This research is focused on investigating the effect of Lactobacillus paracasei ZFM 54 (CCTCC NO:2016667) on attenuating H. pylori-induced gastritis. H. pylori ZJC03 isolated from a patient with gastritis harbored the virulence genes of vacA and cagA and was highly resistant to metronidazole (MIC > 256 µg/mL). In vitro analysis revealed that the potential anti-H. pylori characteristics of L. paracasei ZFM54 in terms of 65.57 ± 1.87% survival rate in simulated gastric juices at a pH of 2.0, 69.00 ± 2.73% auto-aggregation, 30.28 ± 2.24% co-aggregation, 70.27 ± 2.23% urease inhibition, and 57.89 ± 1.27% radical scavenging. In H. pylori infectious mice, L. paracasei ZFM54 pre- and post-treatment reduced the levels of malondialdehyde in liver tissues to 0.71 ± 0.04 nmol/mgprot (p < 0.05) and 0.70 ± 0.06 nmol/mgprot (p < 0.05), respectively. Glutathione levels were increased to 1.78 ± 0.02 µmol/gprot (p < 0.05) and 1.76 ± 0.52 µmol/gprot (p < 0.05), respectively. L. paracasei ZFM54 significantly inhibited H. pylori-mediated inflammation observed in gastric mucosal repair and downregulated the mRNA expression of pro-inflammatory cytokines IFN-γ, IL-1ß, and IL-6 (p < 0.01). Importantly, L. paracasei ZFM54 increased Firmicutes and Actinobacteriota and decreased the relative abundance of bacterial taxa belonging to Campilobacterota and Proteobacteria. With the preventive and therapeutic administration of L. paracasei ZFM54, significant reductions in the average relative abundance of genera Helicobacter, Muribaculum, Staphylococcus, Lachnospiraceae_NK4A136_group, Prevotellaceae_UCG-001, Alloprevotella, and Oscillibacter were observed compared to infected mice. These findings suggest that L. paracasei ZFM 54 has the potential to protect against H. pylori infection by ameliorating inflammation and restoring the gastric microbiota.

Lactobacillus plantarum ZJ316 Attenuates Helicobacter pylori-Induced Gastritis in C57BL/6 Mice.

Helicobacter pylori is a highly prevalent human-specific pathogen that causes various gastric diseases. In the present study, Lactobacillus plantarum ZJ316, which could survive well in simulated gastrointestinal conditions, was found to have significant anti-H. pylori ability. Animal assays revealed that L. plantarum ZJ316 had preventive and therapeutic effects on H. pylori-induced gastritis. L. plantarum ZJ316 significantly decreased interferon γ (IFN-γ) and interleukin 6 (IL-6) levels, increased the IL-10 level, and repaired mucosal damage. Moreover, 16S rRNA gene sequencing revealed that the relative abundance of H. pylori could be significantly reduced by L. plantarum ZJ316 administration. Members of the families Dehalobacteriaceae and Geodermatophilaceae were more prevalent in the prevention group, while Lactobacillaceae and Actinomycetaceae were more prevalent in the treatment group. These results indicate that L. plantarum ZJ316 serves as a potential candidate for the prevention and treatment of H. pylori-induced gastritis by regulating the gastric microbiota and reducing mucosal inflammation.

Phenyl lactic acid alleviates Samonella Typhimurium-induced colitis via regulating microbiota composition, SCFA production and inflammatory responses.

Colitis caused by non-typhoidal Salmonella (NST) infection is increasingly serious and widespread, so new effective treatment strategies with little or no side-effects are urgently needed. Our previous research found that phenyl lactic acid (PLA) derived from Lactobacillus plantarum ZJ316 can effectively inhibit Salmonella enterica Typhimurium (S. Typhimurium). In this study, we further investigated the protective effects of this PLA against S. Typhimurium-induced colitis in mice. An infection model was established using female C57BL/6J mice by oral administration of 109 CFU mL-1 of S. Typhimurium, and PLA was supplied for 10 days after infection. In colitic mice, PLA administration reduced the disease activity index, prevented the colon shortening and spleen enlargement, decreased liver enzyme (AST and ALT) activities, and alleviated the colonic tissue damage. RT-qPCR analysis showed that PLA significantly down-regulated the levels of NF-κB, TLR4 and pro-inflammatory cytokines (IFN-γ, IL-1ß and TNF-α), but stimulated the mRNA expression of the anti-inflammatory cytokine IL-10. Changes in intestinal microecology were analyzed by 16S rRNA sequencing. PLA modulated colonic microbiota dysbiosis by increasing the abundance of Lactobacillus, Butyricicoccus and Roseburia, and reducing Salmonella and Alloprevotella at the genus level. In addition, PLA significantly increased the concentrations of short-chain fatty acids (SCFAs) in the colon, especially propionic acid and butyric acid. These findings revealed that PLA has potential benefits on alleviating S. Typhimurium-induced colitis mainly through intestinal microbiota regulation and inflammation elimination, providing a new perspective for the NTS infection treatment strategy.