Importance of host response for the development of chronic gastritis induced by infection with Helicobacter pylori.

幽门螺杆菌是一种革兰氏阴性的细胞外细菌，参与慢性胃炎和胃癌的发展。我们现在知道，标准的治疗方法是使用抗生素和质子泵抑制剂来预防幽门螺杆菌的胃病。然而，我们也遇到了许多对治疗产生耐药性并再次感染的病例。在这里，我们研究了宿主对幽门螺杆菌的反应是否以及如何参与这些疾病的发展。我们发现幽门螺杆菌感染小鼠慢性胃炎炎症部位有大量嗜酸性粒细胞浸润。此外，IL-33是一种通过诱导IL-13/IL-5和嗜酸性粒细胞趋化因子激活和募集嗜酸性粒细胞的强效细胞因子，在慢性胃炎的发展中是必不可少的。事实上，Il33r^<-/->小鼠对幽门螺杆菌感染引起的慢性胃炎有抵抗力，并且对细菌的清除能力受损。这些结果表明IL-33可能是预防慢性胃炎和胃癌的有效靶点。

Helicobacter pylori is a Gram-negative, extracellular bacterium and is involved in the development of chronic gastritis and gastric cancer. We now know that the standard therapy against H.pylori using antibiotics and proton pomp inhibitor are beneficial for prevention of the gastric diseases. However, we have faced upon many cases that are resistant to the therapy and suffer from the re-infection. Here, we investigated whether and how host responses against H.pylori are involved in the development of those diseases. And we found that many eosinophils are infiltrated in the inflammatory sites of chronic gastritis in H. pylori-infected mice. Furthermore, IL-33, a potent cytokine triggering activation and recruitment of eosinophils via induction of IL-13/IL-5 and chemokines for eosinophils, is essentially required for the development of chronic gastritis. Indeed, Il33r^<-/-> mice are resistant to chronic gastritis induced by infection with H. pylori and are impaired in the clearance of the bacterium. These results indicated IL-33 as a potent target for protection against the chronic gastritis and plausibly gastric cancer.