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.
PLA alleviates S. Typhimurium-induced colitis via decreasing the spleen enlargement and liver enzyme (AST and ALT) activities, and regulating microbiota, SCFA metabolism and inflammatory levels.
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-1β, 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.
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