H. pylori is recognized as a primary etiologic factor in the pathogenesis of gastric disease. Here, we assessed the effect of intragastric administration of H. pylori lipopolysaccharide at 50 and 200 micrograms dose on the epithelial cell apoptosis. Histological examination of the mucosal tissue two days following the treatment revealed that lipopolysaccharide at both doses induced in the rat stomach mucosal inflammatory responses typical of gastritis. The in situ DNA fragmentation assay demonstrated that these changes were associated with a marked increase in gastric epithelial cell apoptosis. The apoptotic index in the controls averaged 0.3%, and increased dramatically to 59% with the lipopolysaccharide at 50 micrograms dose, while at the 200 micrograms dose the apoptotic index of 71.9% was attained. The results point towards cell wall lipopolysaccharide as a virulence factor responsible for the induction of gastric epithelial cell apoptosis by H. pylori.
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