Role of Tumor Necrosis Factor‐Alpha and Interferon‐Gamma in Helicobacter pylori Infection
Role of Tumor Necrosis Factor‐Alpha and Interferon‐Gamma in Helicobacter pylori Infection
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DOI：
10.1111/j.1348-0421.2004.tb03474.x
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发表时间：
2004-09
影响因子：
2.6
通讯作者：
Toshiro Yamamoto;M. Kita;T. Ohno;Y. Iwakura;K. Sekikawa;J. Imanishi
中科院分区：
文献类型：
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作者：
Toshiro Yamamoto;M. Kita;T. Ohno;Y. Iwakura;K. Sekikawa;J. Imanishi
幽门螺杆菌感染的免疫应答在胃十二指肠疾病中起重要作用。采用TNF‐α基因敲除（TNF‐α−/−）小鼠和IFN‐γ基因敲除（IFN‐γ−/−）小鼠研究肿瘤坏死因子α （TNF‐α）和干扰素- 7 （IFN‐γ）诱导胃炎症和保护幽门螺杆菌感染的作用。我们首先检测了幽门螺杆菌菌株CPY2052在C57BL/6野生型和敲除型小鼠胃中的定殖能力。IFN‐γ−/−和TNF‐α−/−小鼠胃中幽门螺杆菌的定植数量高于野生型小鼠。这些发现提示TNF‐α和IFN‐γ可能在幽门螺杆菌感染中发挥保护作用。此外，我们还研究了TNF‐α和IFN‐γ在胃炎症中的作用。与野生型小鼠一样，CPY2052感染的TNF - α - / -小鼠表现出适度的胃固有层单核细胞浸润和胃上皮侵蚀，而CPY2052感染的IFN - γ - / -小鼠在感染后6个月未出现炎症。这些结果表明IFN‐γ可能在幽门螺杆菌感染引起的胃炎症中发挥重要作用，而TNF‐α可能不参与炎症反应的发展。
Immune responses to Helicobacter pylori infection play important roles in gastroduodenal diseases. The contributions of tumor necrosis factor‐α (TNF‐α) and interferon‐7 (IFN‐γ) to the induction of gastric inflammation and to the protection from H. pylori infection were investigated using TNF‐α gene‐knockout (TNF‐α−/−) mice and IFN‐γ gene‐knockout (IFN‐γ−/−) mice. We first examined the colonizing ability of H. pylori strain CPY2052 in the stomach of C57BL/6 wild‐type and knockout mice. The number of H. pylori colonized in the stomach of IFN‐γ−/− and TNF‐α−/− mice was higher than that of wild‐type mice. These findings suggest that TNF‐α and IFN‐γ may play a protective role in H pylori infection. Furthermore, we examined the contribution of TNF‐α and IFN‐γ to gastric inflammation. The CPY2052‐infected TNF‐α−/− mice showed a moderate infiltration of mononuclear cells in the lamina propria and erosions in the gastric epithelium as did wild‐type mice, whereas the CPY2052‐infected IFN‐γ−/− mice showed no inflammatory findings even 6 months after infection. These results demonstrate that IFN‐γ may play an important role in gastric inflammation induced by H. pylori infection, whereas TNF‐α may not participate in the development of inflammatory response.