THE ENDOTOXIN OF HELICOBACTER-PYLORI IS A MODULATOR OF HOST-DEPENDENTGASTRITIS

Atrophic gastritis caused by Helicobacter pylori is the precursor lesi on in the development of intestinal-type gastric adenocarcinoma. In an imal models, atrophic gastritis induced by Helicobacter felis has been shown to be host dependent, developing in some mouse strains and not in others. The lipopolysaccharide (LPS) of H. pylori has been suggeste d to play a role in the induction of gastritis. The goal of this study was to compare the inflammation induced by long-term infection of the C3H/He and the C3H/HeJ strains of mice with H. felis. C3H/HeJ mice ar e unresponsive to LPS. Six months after infection, severe atrophic gas tritis had developed in the body mucosae of all infected C3H/He mice, with replacement of parietal and chief cells. Atrophy was associated w ith a loss of the H. felis from the antral mucosa. In contrast, no atr ophy was seen in the infected C3H/HeJ non-LPS responder animals, and h eavy colonization of the antrum remained. There were no significant di fferences between both the quantitative and qualitative serum immunogl obulin G (Igc) and salivary IgA levels in both strains of mice. The ma in difference between the two strains of long-term-infected mice was a lack of macrophage infiltration in the lamina propria. Immunization i nduced good protective immunity to challenge with viable H. felis. Hel icobacter-induced, host-dependent gastritis is likely to be cell media ted. The C3H/He and C3H/HeJ mouse model provides an excellent opportun ity to investigate the cellular basis of atrophic gastritis.