| Project/Area Number |
23390107
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Bacteriology (including Mycology)
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| Research Institution | Hyogo Medical University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
NAKANISHI Kenji 兵庫医科大学, 医学部, 教授 (60172350)
UCHIYAMA Ryosuke 兵庫医科大学, 医学部, 講師 (20456891)
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| Project Period (FY) |
2011-04-01 – 2014-03-31
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥19,760,000 (Direct Cost: ¥15,200,000、Indirect Cost: ¥4,560,000)
Fiscal Year 2013: ¥5,720,000 (Direct Cost: ¥4,400,000、Indirect Cost: ¥1,320,000)
Fiscal Year 2012: ¥5,720,000 (Direct Cost: ¥4,400,000、Indirect Cost: ¥1,320,000)
Fiscal Year 2011: ¥8,320,000 (Direct Cost: ¥6,400,000、Indirect Cost: ¥1,920,000)
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| Keywords | IL-33 / ヘリコバクターピロリ / 慢性胃炎 / 好酸球 / IL-33受容体 / 自然リンパ球 / IL-13 / インターロイキン３３ / インターロイキン３３受容体 / インターロイキン１３ / インターフェロンγ / Th1細胞分化 / II型自然免疫細胞 / Th１細胞 / インターフェロンガンマ / IL-33受容体(ST2) |
|---|
| Research Abstract |
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.
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