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Helicobacter pylori adhesion molecules, or adhesins, are specialized surface proteins that mediate the attachment of the bacterium to the gastric mucosa, a critical step for persistent colonization and pathogenesis. Key members 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: PubMed, PMID: 11514615). These interactions allow H. pylori to resist the mechanical clearing forces of the stomach and facilitate the delivery of virulence factors like CagA and VacA into host cells (Source: UniProt, P0C688). Other significant adhesins include HopQ, which binds to host CEACAM receptors, and the adherence-associated lipoproteins AlpA and AlpB (Source: Nature Communications, DOI: 10.1038/ncomms14460). By anchoring the bacteria to the epithelium, these molecules contribute to chronic inflammation, peptic ulcers, and an increased risk of gastric cancer (Source: PubMed, PMID: 31736911). Targeting these adhesins with small molecules, carbohydrate mimetics, or vaccines represents a promising therapeutic strategy to prevent or eradicate H. pylori infections without the broad-spectrum impact of traditional antibiotics. Current research focuses on developing multivalent inhibitors that can block multiple adhesin-receptor interactions simultaneously to overcome the high genetic variability of the bacterium (Source: Frontiers in Microbiology, DOI: 10.3389/fmicb.2019.02531).
Anti-adhesion therapy involves the use of receptor analogues, carbohydrate mimetics, or specific antibodies to competitively block the binding sites of H. pylori adhesins, thereby preventing the bacteria from attaching to the gastric mucosa and facilitating their clearance from the stomach (Source: PubMed, PMID: 31736911).
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