pylori during the initiation of acquired immunity (Nagai et al., 2007). However, our previous study demonstrated that H. suis infection induces the formation of gastric lymphoid follicles via a PP-independent pathway, unlike H. pylori infection (Nobutani et al., 2010). From previous reports and our findings, it is suggested that H. suis colonization directly leads to immune responses
in the gastric mucosa and that the development of lymphoid follicles produced by H. suis infection is regulated by local CD4-positive T cells and DC. IFN-γ seems to play an indispensable role in H. suis-induced follicular gastritis. In humans and mice, gastritis induced by H. pylori infection is considered to be a predominantly Th1-mediated disease. In patients infected with H. pylori, the Poziotinib supplier number of CD4-positive T cells was increased in the gastric mucosa, and furthermore, isolated gastric T cells produced cytoplasmic IFN-γ
(Bamford et al., 1998). In addition, IFN-γ production from gastric and splenic T cells has been shown to be upregulated in C57BL/6J WT mice infected with H. pylori, and IFN-γ−/− mice did not develop gastric inflammation despite the colonization of their stomachs by H. pylori (Smythies et al., 2000). In contrast to H. pylori, there are few reports about the Th cytokine profile during H. suis infection. This can be partly explained by the inability to perform immunological analysis; for example a recall assay using splenocytes and the recombinant protein, because the genome sequence of H. suis had not been examined until very recently. Park et al. (2008) reported that the mRNA expression Farnesyltransferase levels of IFN-γ Sunitinib cost and IL-10 in the gastric mucosa were enhanced in ‘H. heilmannii’-infected mice, suggesting that both the Th1 and Th2 responses play roles in the gastric inflammatory responses induced by H. heilmannii’.
In our study, the IFN-γ mRNA expression level was significantly higher in the H. suis-infected C57BL/6J WT mice than in the noninfected mice at 12 weeks after infection (Fig. 5a). Moreover, no gastric lymphoid follicles were detected in the H. suis-infected IFN-γ−/− mice (Fig. 6). On the other hand, the increases in the mRNA expression levels of IL-4 and IL-10 observed in the mice after H. suis infection were small (Fig. 5), and gastric lymphoid follicles were seen in the H. suis-infected IL-4−/− mice, similar to the H. suis-infected IL-4+/− mice (Fig. 7). These results indicate that IFN-γ is involved in the aggregation of follicular lymphocytes, and furthermore, that the Th1 immune response predominantly participates in H. suis strain TKY infection. In contrast, Flahou et al. (2010) reported that gastric inflammation induced by H. suis obtained from pig was more severe in BALB/c mice, which have been known as predominant Th2 responders, compared with C57BL/6J mice, which are considered as predominant Th1 responders at 8 months after infection. Differences in the H.