The role of Helicobacter pylori LPS in the pathogenesis of H. pylori-related gastropathy

Abstract

Helicobacter pylori strains and/or their lipopolysaccharides (LPS) represent the trigger of different regional and systemic immune responses in the course of H. pylori-related gastropathy as indicated by the following: (i) in patients with chronic gastritis (CG) or duodenal ulcer (DU), eradication of H. pylori leads to a dramatic decrease of gastric mucosal content of various cytokines such as interleukin-1β and transforming growth factor-β1; (ii) gastric epithelial cells are activated by H. pylori organisms through tyrosine phosphorylation signaling events but H. pylori LPSs do not affect this signal transduction pathway; and (iii) in sera from patients with CG and DU, besides antibodies to S-form LPS, humoral IgG and IgA response against R-form LPS has been also detected. On the other hand, antibodies against synthetic polymeric Lewis(x) were found in a few patients with CG and in no patients with DU.