Postbiotics Suppress Helicobacter pylori Adhesion and Survival through a Coaggregation Mechanism

Helicobacter pylori can cause gastric ulcers, gastritis, and even gastric Cancer, with increasing Antibiotic resistance. Due to their safety, stability, and lack of side effects, postbiotics have become a focus in H. pylori research. However, strategies for screening anti-H. pylori postbiotics remain unclear. In this study, we used artificial gastric juice and the AGS cell model combined with laser confocal microscopy and scanning electron microscopy to screen for anti-H. pylori postbiotics. The results showed that Lactobacillus rhamnosus MN45 had the strongest coaggregation with H. pylori, significantly inhibited H. pylori-induced Urease activity, virulence factor expression, and inflammatory response. The coaggregation phenomenon increased over time and remained stable in an acidic environment. Comparative genomic analysis revealed that the amplification of COG1396 in MN45 may potentiate XRE-mediated signaling and upregulate adhesion factor biosynthesis, thereby improving its coaggregation capacity with H. pylori. This study provides new insights into the postbiotic-mediated coaggregation mechanism of H. pylori.

Helicobacter pylori; adhesion; coaggregation; postbiotics; virulence.