Helicobacter pylori adhesion to gastric epithelium and surface polymers

Helicobacter pylori adhesion to the gastric epithelium and surface polymers is a fundamental mechanism for the persistent colonization of the human stomach. This interaction is primarily mediated by bacterial outer membrane proteins called adhesins, such as BabA (Blood group antigen-binding adhesin) and SabA (Sialic acid-binding adhesin), which bind to specific carbohydrate motifs like Lewis b and sialyl-Lewis x on host cells (Ilver et al., 1998; Mahdavi et al., 2002). Successful adhesion allows the bacterium to resist the flushing action of gastric motility and mucus turnover, facilitating the delivery of toxins like CagA into the host epithelium (Polk & Peek, 2010). This process is a major driver of chronic inflammation, leading to clinical outcomes such as peptic ulcers and gastric adenocarcinoma (Wroblewski et al., 2010). Therapeutic strategies targeting this process, known as anti-adhesion therapy, aim to displace or prevent the binding of H. pylori using competitive inhibitors like bismuth salts or specific oligosaccharides (Wagstaff et al., 1988). Unlike traditional antibiotics, anti-adhesion agents may reduce the risk of developing systemic antibiotic resistance while specifically clearing the infection from the gastric niche.

Other names

H. pylori gastric adhesionHelicobacter pylori mucosal attachmentH. pylori-host cell interaction

Competitive inhibition of bacterial adhesins (e.g., BabA, SabA) binding to host cell surface glycoconjugates.