ABSTRACT
Helicobacter pylori are able to agglutinate erythrocytes from a large variety of mammalian species. There is strong evidence that H. pylori specifically colonize the surface of the gastric mucosal epithelium. In the case of gastric metaplasia, histological studies show that the junction between the normal and ectopic gastric epithelium precisely defines the limit of H. pylori intestinal colonization. A soluble hemagglutinin of similar but distinct specificity has also been described for some strains of H. pylori. Several laboratories have reported other glycolipid receptors for H. pylori, and it is thus likely that host cell attachment is a multifactorial process. The concept of SGT binding by H. pylori is interesting since such glycolipids have been shown to be preferentially present in intestinal epithelial cells frequently exposed to acid. Several cell adhesion studies have been consistent with the involvement of a lipid receptor in H. pylori host cell attachment.
