Bacterial adhesion to gastric epithelial cell

Bacterial adhesion to gastric epithelial cells is the initial step whereby bacteria such as *Helicobacter pylori* attach to the mucosal lining of the stomach via specialized bacterial outer membrane proteins (adhesins) that recognize and bind to specific glycan structures on the host cell surface, including mucins and blood group antigens. Key bacterial adhesins involved include BabA (binding to Lewis b antigen), SabA (binding to sialyl-Lewis antigens), as well as several others (AlpA/B, HopQ, HopZ, OipA). This adhesion process is crucial for successful colonization, immune evasion, persistent infection, delivery of bacterial toxins (such as CagA), and subsequent disease pathogenesis (chronic gastritis, peptic ulcers, and gastric cancer). Disruption of this adhesion (by, e.g., probiotics, glycan analogs, or small molecules) has been explored as a therapeutic strategy, but no approved drugs specifically target this process as a unique molecular entity[1][2][4].