Helicobacter pylori adhesion to gastric epithelium

Helicobacter pylori adhesion to the gastric epithelium is a fundamental step in the establishment of chronic infection and subsequent gastric disease (Kusters et al., 2006). This process is mediated by a variety of bacterial outer membrane proteins, termed adhesins, which recognize specific carbohydrate receptors on the host cell surface (Ishijima et al., 2011). The most well-characterized interaction involves the Blood group antigen-binding adhesin (BabA) binding to the Lewis b (Leb) antigen on gastric epithelial cells (Aspholm-Hurtig et al., 2004). Another key adhesin, Sialic acid-binding adhesin (SabA), mediates binding to sialyl-Lewis x antigens, which are typically induced during gastric inflammation (Mahdavi et al., 2002). These interactions allow the bacteria to resist the mechanical clearing forces of the stomach and facilitate the localized delivery of toxins like CagA and VacA. Because adhesion is essential for virulence, it is considered a high-value therapeutic target for anti-adhesive agents (Sykora et al., 2005). Such agents, including carbohydrate mimetics and specific antibodies, aim to competitively inhibit these bindings to prevent colonization or displace existing bacteria. This approach offers a potential alternative or adjunct to traditional antibiotic therapy, particularly in the face of rising multi-drug resistance in H. pylori strains.

Other names

Helicobacter pylori attachmentGastric colonizationBabA-mediated adhesionSabA-mediated adhesion

Competitive inhibition of bacterial adhesins (e.g., BabA, SabA) binding to host gastric epithelial receptors (e.g., Lewis b, sialyl-Lewis x).