Induction of follicular gastritis following postthymectomy autoimmune gastritis in Helicobacter pylori-infected BALB/c mice

Helicobacter pylori is the major causative agent of chronic antral gastriti s and is thought to be involved in the pathogenesis of mucosa-associated ly mphoid tissue lymphoma (MALToma) developing in the human stomach. The aim o f this study was to clarify whether corporal autoimmune gastritis (AIG), wh ich is known to decrease acidity due to destruction of parietal cells, pred isposes mice to H. pylori infection, thereby leading to MAL-Toma-like patho logy, BALB/c mice in which AIG had been induced by thymectomy 3 days after birth (AIG mice) were used. The AIG mice were orally administered mouse-ada pted H. pylori at the age of 6 weeks and were examined histologically and s erologically after 2 to 12 months. The results were compared with those obt ained from uninfected AIG mice and infected normal mice, Germinal centers w ere induced in the corpus in 57% of the N. pylori-infected AIG mice, which elicited anti-H. pylori antibody responses in association with upregulation of interleukin-4 (IL-4) mRNA. In these mice, parietal cells remained in th e corpus mucosa. These findings were in contrast to those with the uninfect ed AIG mice: fundic gland atrophy due to disappearance of parietal cells as sociated with upregulation of gamma interferon, but not IL-4, mRNA and no g erminal center formation in the corpus. These observations suggest that AIG alters the infectivity of H. pylori, leading to MALToma-like follicular ga stritis, at an early stage after H. pylori infection.