Publications

the sialic acid binding saba adhesin of helicobacter pylori is essential for nonopsonic activation of human neutrophils.	infiltration of neutrophils and monocytes into the gastric mucosa is a hallmark of chronic gastritis caused by helicobacter pylori. certain h. pylori strains nonopsonized stimulate neutrophils to production of reactive oxygen species causing oxidative damage of the gastric epithelium. here, the contribution of some h. pylori virulence factors, the blood group antigen-binding adhesin baba, the sialic acid-binding adhesin saba, the neutrophil-activating protein hp-nap, and the vacuolating cytotoxi ...	2005	15689619
helicobacter pylori induces beta3gnt5 in human gastric cell lines, modulating expression of the saba ligand sialyl-lewis x.	chronic helicobacter pylori infection is recognized as a cause of gastric cancer. h. pylori adhesion to gastric cells is mediated by bacterial adhesins such as sialic acid-binding adhesin (saba), which binds the carbohydrate structure sialyl-lewis x. sialyl-lewis x expression in the gastric epithelium is induced during persistent h. pylori infection, suggesting that h. pylori modulates host cell glycosylation patterns for enhanced adhesion. here, we evaluate changes in the glycosylation-related ...	2008	18483624
muc1 limits helicobacter pylori infection both by steric hindrance and by acting as a releasable decoy.	the bacterium helicobacter pylori can cause peptic ulcer disease, gastric adenocarcinoma and malt lymphoma. the cell-surface mucin muc1 is a large glycoprotein which is highly expressed on the mucosal surface and limits the density of h. pylori in a murine infection model. we now demonstrate that by using the baba and saba adhesins, h. pylori bind muc1 isolated from human gastric cells and muc1 shed into gastric juice. both h. pylori carrying these adhesins, and beads coated with muc1 antibodies ...	2009	19816567