AI Insight
This study investigated the anti-Helicobacter pylori properties of the probiotic strain Lactobacillus casei HY001 through both laboratory and animal experiments. In vitro, HY001 inhibited H. pylori growth, reduced urease activity, demonstrated co-aggregation with the pathogen, and blocked its adhesion to gastric epithelial cells. In animal models, HY001 attenuated gastric inflammation by suppressing NF-kB signaling and lowering pro-inflammatory cytokines, while also partially restoring the gastric microbiota diversity and community structure disrupted by H. pylori infection.
Why it matters
H. pylori infects approximately half of the global population and is a leading cause of gastric ulcers and stomach cancer, making probiotic-based adjunct therapies a clinically relevant area of research. If validated in human trials, L. casei HY001 could offer a supplementary strategy to reduce reliance on antibiotics and address growing antimicrobial resistance concerns in H. pylori treatment.
by Zhonghua Lv, Junqing Yu, Xueting Zhang, Lei Zhang, Chunlei Zhang, Xiaoxu Liu, Yu Chang, Hang Yin, Wei Wang, Haidan Zhao, Huicheng Li
Helicobacter pylori (H. pylori) is a highly pathogenic microorganism that can cause various gastric diseases. Accumulating evidences have demonstrated probiotics’ potential in combating H. pylori infections. The aim of this study was to explore the effects and underlying mechanism of Lactobacillus casei (L. casei) HY001 against the gastric inflammation and gastric microbiota alteration induced by H. pylori infection. These results indicated that L. casei HY001 significantly inhibited the growth of H. pylori SS1, decreased urease activity, and exhibited strong co-aggregation properties with H. pylori SS1 in vitro experiments. Furthermore, L. casei HY001 was found to be capable of inhibiting the adhesion of H. pylori SS1 with AGS cells. Subsequently, Experiments in animals suggested L. casei HY001 alleviated gastric inflammation by inhibiting the expression of NF-κ B and reducing pro-inflammatory mediator levels (IL-8, TNF-α, IL-1β, and IL-6). Moreover, the gastric microbiota 16S rRNA gene sequencing analysis revealed that L. casei HY001 improved the structure of the gastric microbiota by modulating the abundance of Firmicutes, Bacteroidota and Proteobacteria. Meanwhile, the relative abundances of Rothia, Clostridium-sensu-stricto-1, Alistipe and Prevotellacea-UG-001 were significantly increased. In contrast, the abundances of Helicobacter, Turicibacter, unclassified – Muribaculaceae, unclassified- Oscillospiraceae and Lachnospiraceae -NK4A136-group were significantly reduced following HY001 intervention. These researches indicated that L. casei HY001 improved H. pylori SS1 induced gastric mucosal damage in mice, regulated immune factors, enhanced the reduced diversity of gastric Lachnospiraceae microbiota caused by H. pylori infection, and restored the stability of the microbial community structure.