Importance of host response for the development of chronic gastritis induced by infection with Helicobacter pylori.
Importance of host response for the development of chronic gastritis induced by infection with Helicobacter pylori.
批准号:
20390129
负责人:
TSUTSUI Hiroko
金额:
$12.48万
依托单位国家:
日本
项目类别:
Grant-in-Aid for Scientific Research (B)
财政年份:
2008
资助国家:
日本
项目状态:
已结题
起止时间:
2008 至 2010
中文摘要
幽门螺杆菌是一种革兰氏阴性的细胞外细菌,与慢性胃炎和胃癌的发生有关。我们现在知道,使用抗生素和质子泵抑制剂的标准治疗幽门螺杆菌对预防胃病是有益的。然而,我们面对许多病例对治疗产生耐药性,并遭受再感染。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。在H. pylori感染的小鼠此外,IL-33是一种通过诱导IL-13/IL-5和嗜酸性粒细胞趋化因子而触发嗜酸性粒细胞活化和募集的强效细胞因子,其是慢性胃炎发展所必需的。事实上,Il 33 r ^<-/->小鼠对由H.幽门螺杆菌和受损的清除细菌。这些结果表明IL-33是预防慢性胃炎和胃癌的有效靶点。
英文摘要
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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TLR4 介导的 caspase-1 激活需要 MyD88 和 TRIF
DOI:
--
发表时间:
2008
期刊:
影响因子:
--
作者:
[Imamura, M., Tsutsui, H., Yasuda, K., Akira, S., Fujimoto, J., Nakanishi K.]
通讯作者:
Nakanishi K.
Neutrophil-dominant psoriasis-like inflammation induced by epidermal-specific expression of Raf in mice.
Raf 表皮特异性表达在小鼠中诱导中性粒细胞为主的银屑病样炎症。
DOI:
--
发表时间:
2010
期刊:
J.Dermatol. Sci. 58
影响因子:
--
作者:
[Tarutani, M., Imai, Y., Yasuda, K., Tsutsui, H., Nakanishi, K., Yamanishi K.]
通讯作者:
Yamanishi K.
Vibrio vulnificus activates Nalp3 inflammasome via the synergistic action of pore formation toxins.
创伤弧菌通过孔形成毒素的协同作用激活 Nalp3 炎症小体。
DOI:
--
发表时间:
2008
期刊:
影响因子:
--
作者:
[Toma, C., Higa, N., Nakasone, N., Koizumi, Y., McCoy, A. J., Ogura, Y., Tsutsui, H., Matsumoto, J., Franchi, L., Nunez, T., Suzuki, T.]
通讯作者:
T.
アレルギー疾患の免疫機構
过敏性疾病的免疫机制
DOI:
--
发表时间:
2009
期刊:
影响因子:
--
作者:
[Seto S, Matsumoto S, Tsujimura K, Koide Y, 川口寧, 筒井ひろ子]
通讯作者:
筒井ひろ子
Helicobacter pylori感染マウスモデルにおけるIL-33依存的な菌の排除機構
幽门螺杆菌感染小鼠模型中 IL-33 依赖性细菌清除机制
DOI:
--
发表时间:
2010
期刊:
影响因子:
--
作者:
[今村美智子, 筒井ひろ子, 藤元治朗, 中西憲司, 田中正視, 江崎孝行, 福田典子,内山良介,筒井ひろ子]
通讯作者:
福田典子,内山良介,筒井ひろ子
共 17 条
Interferon-gamma-mediated tissue factor expression contributes to T-cell-mediated fulminant hepatitis through induction of hyper coagulation in mice
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Roles of IL-33 in the development of gastritis of Helicobacter pylori-infected mice
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Inflammatory response-mediated Hypercoagulation underlies Concanavalin A-induced severe hepatitis in mice
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财政年份:2010
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Treatment of endotoxin-induced tissue damages by the negative regulation of TLR-mediated signal pathways
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