Roles of IL-33 in the development of gastritis of Helicobacter pylori-infected mice

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Helicobacter pylori is a Gram-negative spillilum and causes chronic gastritis, peptic ulcer, and gastric cancer in human. It is important to know how the bacterium induces gastric cancer. Deletion of pathogenic factor CagA considerably dampens its ability to induce gastritis in mice, indicating the importance of CagA for the gastric alterations. However, mice deficient in Th1 cell ability can evade the disease even after infection with CagA-positive bacterium. This clearly indicates that host response profoundly participates in the development of gastritis. Here, we found that IL-33 signaling is required for the development of gastritis in mice. In particular, mice deficient in IL-33 or its receptor do not have potential to differentiate into H. pylori-speicific Th1 cells. These results suggest that IL-33 signaling might be the target for treatment of H. pylori-induced chronic gastric alterations including gastric cancer.