Sucralfate counteracts the inhibition of gastric mucosal mucin receptor by helicobacter pylori lipopolysaccharide

Background: Among the disturbances in gastric mucosal defense associated with Helicobacter pylori infection is the loss of mucus coat continuity, which results in a severe disturbance in the ability of mucus coat to maintain its functions as the pre-epithelial element of gastric mucosal defense. Here, we show that H. pylori, through its cell-wall lipopolysaccharide, disrupts the interaction between gastric mucin and its mucosal receptor, and that sucralfate is capable of counteracting this untoward effect of the bacterium. Methods: The receptor was isolated from octylglucoside-solubilized gastric mucosal epithelial cell membranes by affinity chromatography on Sepharose-bound wheat germ agglutinin and following iodination with ¹²⁵I, used in the binding assays for mucin in the presence of H. pylori lipopolysaccharide and sucralfate. Results: Preincubation of the receptor protein with H. pylori lipopolysaccharide led to a decrease in mucin binding. The inhibitory effect was proportional to the concentration of lipopolysaccharide and reached a maximum of 91% at 30 μg/ml. The effect of H. pylori lipopolysaccharide was countered by sucralfate, which caused a dose-dependent relief of the inhibitory effect. The maximum (75% restoration in mucin-receptor binding occurred at 60 μg/ml sucralfate. Conclusions: The results provide strong evidence for the effectiveness of sucralfate in preventing the loss of gastric mucus coat continuity caused by H. pylori.