BIOCHEMICAL ASPECTS OF HELICOBACTER-PYLORI COLONIZATION OF THE HUMAN GASTRIC-MUCOSA

Unlike Helicobacter felis and other Helicobacter species of animal ori gin, Helicobacter pylori colonizes the lower gastric mucin layer of th e stomach and adheres to human gastric epithelial cells. It is still a n open question if H. pylori can interact with specific glycoconjugate s in the gastric mucin layer. It is possible that colonization of the oral cavity is a first step of a complex infectious process. Most like ly resting or slow growing cells of H. pylori interact with Lewis bloo d group substances in the gastric mucin layer and on the epithelium. T his initial colonization is probably followed by binding to specific c ell surface glycoconjugates (glycoproteins and glycolipids such as GM( 3)) and specific sialylated or highly sulphated molecules such as cell surface sulphatides and heparan sulphate, H. pylori may also bind to specific phospholipid molecules such as phosphatidyl-ethanolamine on t he gastric cells. The adhesion process of certain strains can stimulat e 'close' cell adhesion including pedestal formation similar to the ph enomenon typical for a special class of enterovirulent Escherichia col i called attaching effacing E. coli. After gastric cell destruction by ammonia and H. pylori toxins (such as the vacuolating toxin) H. pylor i may colonize the extracellular matrix (ECM). This phenomenon seems t o include binding of cell surface sialic acid specific haemagglutinin to one ECM component, i.e. laminin. It is also likely that H. pylori m ay use similar events to penetrate intercellular junctions of gastric epithelial cells. These adhesion-penetration phenomena also involve co ating of the microbe with host proteins to escape the host immune syst em and initiate a chronic lifelong infection process.