| Project/Area Number |
20390129
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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 College of Medicine |
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Principal Investigator |
TSUTSUI Hiroko Hyogo College of Medicine, 医学部, 教授 (40236914)
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| Co-Investigator(Kenkyū-buntansha) |
NAKANISHI Kenji 兵庫医科大学, 医学部, 教授 (60172350)
HAYASHI Shuhei 兵庫医科大学, 医学部, 講師 (40322185)
UCHIYAMA Ryousuke 兵庫医科大学, 医学部, 助教 (20456891)
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| Project Period (FY) |
2008 – 2010
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| Project Status |
Completed (Fiscal Year 2010)
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| Budget Amount *help |
¥19,500,000 (Direct Cost: ¥15,000,000、Indirect Cost: ¥4,500,000)
Fiscal Year 2010: ¥5,720,000 (Direct Cost: ¥4,400,000、Indirect Cost: ¥1,320,000)
Fiscal Year 2009: ¥6,630,000 (Direct Cost: ¥5,100,000、Indirect Cost: ¥1,530,000)
Fiscal Year 2008: ¥7,150,000 (Direct Cost: ¥5,500,000、Indirect Cost: ¥1,650,000)
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| Keywords | 感染免疫 / ヘリコバクター・ピロリ / 好酸球 / インターロイキン33(IL-33) / IL-33 / 受容体 / 胃粘膜上皮細胞 / 好中球 / インターロイキン33 / ST2(IL-33受容体) / Toll様受容体 / カスパーゼ1 / NOD様受容体 / 胃上皮細胞 / 慢性感染 |
|---|
| Research Abstract |
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.
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