Bifidobacterium longum Bianquejun 19 Suppresses Helicobacter pylori Motility and Colonization by Disrupting Energy Metabolism

Abstract The mechanisms by which probiotics interfere with Helicobacter pylori remain incompletely understood. This study systematically evaluated the effects of Bifidobacterium longum Bianquejun 19 on H. pylori -related biological phenotypes and validated these effects using metatranscriptomic analysis, in vitro physiological measurements, and animal experiments. B. longum Bianquejun 19 inhibited the growth of H. pylori . Its fermentation supernatant exhibited strong antibacterial activity both before and after pH neutralization, producing inhibition zones of 19.00–24.00 mm. In the competition model, the bacterial suspension reduced H. pylori adhesion and invasion by up to 71.41% and 73.57% in the competition model, respectively. Metatranscriptomic analysis showed that nine genes associated with central carbon metabolism were downregulated by 1.68–2.49-fold, while 15 genes involved in the respiratory chain were downregulated by 2.00–5.30-fold. Among these, the ATP synthase-related genes atpE and atpD were downregulated by 2.18- and 1.48-fold, respectively. Acetyl-CoA levels initially increased and subsequently decreased, ATP levels declined from 783.33 nmol/10⁴ bacteria at 0 h to 26.22 nmol/10⁴ bacteria at 24 h, and NADH/NAD⁺ homeostasis was disrupted. The key flagellar genes fliN and fliI were downregulated by 1.53- and 1.74-fold, respectively, while the virulence-associated gene cagA was downregulated by 2.14-fold. The motility of H. pylori was markedly impaired: the radius of the motility zone decreased significantly from 11.6 mm to 4.6 mm after 4 h, and no obvious motility zone was observed after 8 h. These changes were accompanied by bacterial deformation and reduced or disrupted flagella. In the mouse infection model, all B. longum Bianquejun 19 intervention groups showed reduced inflammatory infiltration in the gastric mucosa and decreased gastric collagen deposition. Gastric CagA protein levels were significantly reduced in both the bacterial suspension and fermentation supernatant groups. In addition, the colonic short-chain fatty acid profile showed component-dependent improvement. These findings indicate that B. longum Bianquejun 19 disrupts bacterial energy metabolism and motility-dependent colonization while modulating host inflammatory and metabolic responses, thereby alleviating H. pylori -induced collagen deposition in the gastric mucosa.