Helicobacter pylori strains and/or their lipopolysaccharides (LPS) represen
t the trigger of different regional and systemic immune responses in the co
urse of H. pylori-related gastropathy as indicated by the following: (i) in
patients with chronic gastritis (CG) or duodenal ulcer (DU), eradication o
f H. pylori leads to a dramatic decrease of gastric mucosal content of vari
ous cytokines such as interleukin-1 beta and transforming growth factor-bet
a 1, (ii) gastric epithelial cells are activated by H. pylori organisms thr
ough tyrosine phosphorylation signaling events but H. pylori LPSs do not af
fect 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 ag
ainst synthetic polymeric Lewis(x) were found in a few patients with CG and
in no patients with DU.