Helicobacter pylori adhesins and gastric mucosal receptors

Helicobacter pylori adhesion to the gastric mucosa is a fundamental prerequisite for its colonization and the development of associated diseases such as chronic gastritis, peptic ulcers, and gastric adenocarcinoma (Source: Frontiers in Microbiology, 2021; Toxins, 2021). This process is mediated by a sophisticated array of bacterial surface proteins, known as adhesins, which specifically recognize and bind to glycan receptors on the host's gastric epithelial cells and within the mucus layer (Source: Frontiers in Cellular and Infection Microbiology, 2020; NIH, 2021). Key adhesins include the blood group antigen-binding adhesin (BabA), which binds to Lewis b antigens, and the sialic acid-binding adhesin (SabA), which interacts with sialyl-Lewis X antigens (Source: Ace Therapeutics; Toxins, 2021). These interactions not only anchor the bacteria against the mechanical forces of the stomach but also facilitate the delivery of virulence factors, such as CagA, into host cells via the Type IV secretion system (Source: Frontiers in Microbiology, 2021; NIH, 2019). Therapeutic strategies targeting these adhesion sites, known as anti-adhesion therapy, aim to prevent or disrupt bacterial attachment using glycan mimetics, small molecule inhibitors, or mucoprotective agents (Source: ResearchGate, 2021; Science Advances, 2015). This approach is particularly valuable as an alternative or adjunct to traditional antibiotics, potentially reducing the selection pressure for antibiotic resistance and sparing the host's commensal microbiota (Source: ResearchGate, 2021; HCPLive, 2015).

Other names

Helicobacter pylori adhesion sites on gastric mucosa and bacterial surface proteinsH. pylori outer membrane proteinsBabA-Leb complexSabA-sLeX complexBacterial adhesins and host receptorsH. pylori adhesin-receptor interaction

Competitive inhibition of bacterial attachment to gastric epithelial cells by blocking the interaction between bacterial adhesins (e.g., BabA, SabA) and host glycan receptors (e.g., Lewis b, sialyl-Lewis X).