GASTROPROTECTIVE AGENTS IN MUCOSAL DEFENSE AGAINST HELICOBACTER-PYLORI

1. Convincing evidence now exists that infection with H. pylori plays a major role in the pathogenesis of gastric disease. Having a niche bo rdering two major perimeters of mucosal defenses, the bacterium appare ntly exerts its detrimental effect on the mucus layer as well as the g astric epithelium. Therefore, gastroprotective agents capable of count eracting these detrimental effects of H. pylori are gaining importance in the treatment of gastric disease. 2. The colonization of gastric m ucosa by H. pylori involves specific glycolipid receptors bearing acid ic substituents, a process inhibited by gastric sulfomucins. Two antiu lcer agents bearing sulfated sugar groups have been demonstrated to po ssess the ability to interfere with H. pylori colonization process. Th ese are sucralfate and sulglycotide. The two agents are also potent in hibitors of H. pylori glycosulfatase activity directed against indigen ous mucosal defenses. 3. A variety of extracellular enzymes such as pr oteases, lipases and phospholipases, elaborated by H. pylori cause the weakening of the integrity of gastric mucus coat and render the under lying epithelium vulnerable to noxious luminal contents. Among the mos t potent agents capable of countering the proteolytic activity of H. p ylori are nitecapone, ebrotidine and sulglycotide, while ebrotidine an d sulglycotide were found to be most effective inhibitors of H. pylori lipolytic activities. 4. The gastric epithelial integrity is compromi zed by the H. pylori cell-wall lipopolysaccharide untoward effect on t he epithelial surface receptors. The interference of the lipopolysacch aride with the laminin receptor was found to be most efficiently count ered by ebrotidine, sulglycotide and sucralfate, whereas sulglycotide is the most potent in the reversal of the inhibitory effect of the lip opolysaccharide on mucin receptor binding.