Helicobacter pylori adhesin (e.g., BabA, SabA, HopQ, HpaA)

Helicobacter pylori adhesion to epithelial cells refers to the critical initial step in colonization and pathogenesis by this bacterium within the human stomach. This process is mediated primarily by a set of outer membrane proteins known as adhesins, which include well-characterized molecules such as BabA (blood group antigen-binding adhesin), SabA (sialic acid-binding adhesin), HopQ, and HpaA among others. These proteins recognize and bind specifically to glycan structures or cell surface receptors on gastric epithelial cells—BabA binds Lewis b antigens on blood group O individuals, SabA binds sialyl-Lewis x antigens found on inflamed tissue, HopQ interacts with CEACAM family members facilitating CagA translocation into host cells via type IV secretion system, while HpaA has been shown structurally essential for cell binding and can induce pro-inflammatory responses[1][2][4][5][6]. The interaction between these bacterial factors and their corresponding host ligands enables stable colonization despite harsh gastric conditions and underlies chronic infection outcomes including gastritis, ulcers, and increased risk for gastric cancer. Disruption of these interactions—either through small molecule inhibitors or vaccines targeting key epitopes—is an area of active therapeutic research but no direct antiadhesive therapies are currently approved. In summary: "Helicobacter pylori adhesion to epithelial cells" is not itself a molecular target but describes a pathogenic mechanism involving several distinct outer membrane protein targets that mediate attachment between bacterium and host tissue—a prerequisite for infection establishment.[1][4][5]

Other names

H. pylori adhesion proteinsHelicobacter pylori outer membrane proteinsH. pylori OMPs

Inhibition of bacterial adhesion to epithelial cells by blocking adhesin-receptor interactions