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Helicobacter pylori adhesion to gastric epithelial cells is a critical early step in the pathogenesis of H. pylori infection, enabling the bacterium to colonize the human stomach and resist clearance. This process is mediated by specific interactions between bacterial adhesins (e.g., BabA, SabA) and host cell receptors (e.g., Lewis antigens, CEACAMs) on the gastric epithelium, facilitating colonization, virulence factor delivery, and induction of chronic inflammation, which can lead to gastritis, ulcers, or gastric cancer.
Interference with adhesin-receptor binding; disruption of bacterial cell wall integrity; inhibition of bacterial growth.
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