Helicobacter pylori adhesion to gastric epithelial cells is mediated by glycan receptors

The Three-dimensional Structure of the Extracellular Adhesion Domain of the Sialic Acid-binding Adhesin SabA from Helicobacter pylori

“…The ability to attach to the gastric epithelium is crucial for H. pylori to colonize and establish lifelong chronic infection in the host. The sialic acid binding adhesin (SabA) 5 is one of the best characterized H. pylori adhesins (2,3). It belongs to the Hop superfamily of outer membrane proteins, which also includes the Lewis B antigen-binding adhesin, BabA, and the glycoprotein-binding adhesins AlpA and AlpB.…”

Molecular mechanisms and biological role ofCampylobacter jejuniattachment to host cells

“…Host cell interaction in such bacteria such as H. pylori and E. coli may involve interaction of adhesins with oligosac-charides found on the surface of host cells [1,54,55]. A similar lectin-glycan interaction appears to take place in case of Campylobacter.…”

Transfection of the Helicobacter�pylori CagA gene alters MUC5AC expression in human gastric cancer cells

“…Adhesion to the gastric mucosa is important in the life cycle of H. pylori (4). As MUC5AC is an important receptor for gastric mucosa adhesion (5-7), efficient colonization of the stomach requires high expression of MUC5AC by gastric epithelial cells (8,9). Previous studies have demonstrated that the stomach epithelium reacts to H. pylori infection by activating pro-inflammatory signaling pathways (10), thereby activating innate defense mechanisms against H. pylori, which may include the downregulation of MUC5AC expression in the human gastric mucosa (2,6,11,12).…”

“…The association between H. pylori infection and gastric epithelial MUC5AC expression is well-recognized (6)(7)(8)(9)16), there are a limited number of studies regarding the molecular mechanisms that mediate H. pylori-dependent compensatory responses, with respect to host downregulation of MUC5AC mucin gene expression. The downregulation of MUC5AC expression appears to be derived from an epithelial reaction towards the urease virulence factor of H. pylori (17).…”