pylori is 70–80% in Japanese (age >40 years) (Asaka et al., 1992). It seems highly possible that H. heilmannii has a greater tendency to induce gastric MALT lymphoma than other Helicobacter species. For example, a clinical study reported that primary gastric MALT lymphoma occurred more frequently in H. heilmannii-infected patients (1.47%)

than in H. pylori-infected patients (0.66%) (Morgner et al., 2000). In experimental animals, it was also revealed that H. heilmannii infection caused gastric MALT lymphoma in 100% of C57BL/6 mice in a check details 6-month period (Nakamura et al., 2007). On the other hand, Helicobacter felis infection induced gastric MALT lymphoma-like lesions at a 38% incidence in BALB/c mice 22 months after infection (Enno et al., 1995). These two animal experiments also suggest that H. heilmannii infection have a strong potential to induce gastric MALT lymphoma compared with other Helicobacter species, although the genetic and immunological differences of host mice should be investigated. However, it remains to be assessed why there are such differences in the incidence of the development of gastric MALT lymphoma between H. heilmannii and other Helicobacter species. The development of ectopic (tertiary) lymphoid tissues such as gastric lymphoid follicles, which is predisposed toward gastric MALT lymphoma, is closely associated with chronic stimulation by pathogens, such as Helicobacter

Fulvestrant bacteria (Carragher et al., 2008). Previous studies revealed that the activation and proliferation of mucosal B cells in gastric MALT lymphoma, which is typically derived from B cells, were dependent on H. pylori-specific T cells (D’Elios et al., 1999, 2005), suggesting that the acquired immunity

induced by H. pylori infection plays a key role in the development of gastric MALT lymphoma. Recently, Peyer’s patches (PP), which are the major induction site for immune responses to microorganisms and pathogens in the gastrointestinal tract (Newberry & Lorenz, 2005), were reported to play important roles in acquired immunity against Helicobacter bacteria including H. pylori and H. felis. In a PP-deficient mouse (PP null mice) model, chronic gastritis induced by H. pylori or H. felis infection was markedly impaired in comparison with that in wild-type mice (Kiriya et al., 2007; Nagai et al., 2007). However, the involvement of PP Aprepitant in H. heilmannii-induced diseases is still unknown. In this study, the roles of PP in H. heilmannii-induced immune responses and the development of gastric lymphoid follicles in the gastric mucosa were examined using PP null mice, which were generated by the administration of anti-IL-7Rα antibody into C57BL/6J pregnant mice according to the method of a previous report (Yoshida et al., 1999). C57BL/6J wild-type mice and PP null mice were infected with H. heilmannii, and in addition to histological and immunohistological examinations, the expression levels of cytokines and chemokines in the gastric mucosa were investigated.