Helicobacter pylori adhesin-host receptor system (H. pylori adhesin-receptor system)

Helicobacter pylori (H. pylori) adhesion to the gastric mucosa is a critical initial step for successful colonization and persistent infection, mediated by a complex interplay between bacterial surface adhesins and host gastric receptors [1, 2, 3]. Key bacterial adhesins include the blood group antigen-binding adhesin (BabA), which recognizes fucosylated Lewis b (Leb) antigens on healthy mucosa, and the sialic acid-binding adhesin (SabA), which binds to sialyl-Lewis X (sLeX) antigens upregulated during inflammation [5, 6, 7]. Other important factors include HopQ, which interacts with host CEACAMs, and LabA, which binds to gastric mucins like MUC5AC [1, 3]. This adhesion system allows the bacteria to resist mechanical clearance by gastric peristalsis and mucus shedding, while also facilitating the delivery of virulence factors like CagA via the type IV secretion system [13, 18]. Therapeutically, this system is a target for anti-adhesion strategies, including carbohydrate mimetics and mucoprotective agents, which aim to block bacterial attachment and enhance the efficacy of standard antibiotic treatments [4, 10, 15].

Other names

Helicobacter pylori surface adhesins and host gastric glycolipid receptors involved in H. pylori adhesionBabA-Leb interactionSabA-sLeX interactionH. pylori adhesion factorsH. pylori outer membrane proteins

Inhibition of bacterial attachment to the gastric mucosa by blocking adhesin-receptor interactions or mimicking host glycans [4, 10, 15].