Helicobacter pylori gastritis in children is associated with a regulatory T-cell response
Helicobacter pylori gastritis in children is associated with a regulatory T-cell response
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DOI：
10.1053/j.gastro.2007.11.006
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发表时间：
2008-02-01
期刊：
影响因子：
29.4
通讯作者：
Smith, Phillip D.
中科院分区：
文献类型：
--
作者：
Harris, Paul R.;Wright, Shelton W.;Smith, Phillip D.
背景与目的：儿童幽门螺杆菌感染很少引起胃十二指肠粘膜溃疡。由于幽门螺杆菌可诱导成人T细胞依赖的胃炎症，而T调节细胞(Treg)抑制T细胞依赖的病理改变，因此我们对儿童和成人的胃组织病理学和Treg细胞反应进行了评估。方法：采用免疫分析、免疫组织化学和实时聚合酶链式反应等方法，对智利圣地亚哥36例有腹部症状的儿童和79例成人的胃组织进行前瞻性的幽门螺杆菌检测和组织病理学检查。结果：18例(50%)儿童和51例成人(65%)感染幽门螺杆菌。儿童和成人的幽门螺杆菌感染水平相似。然而，与成人相比，儿童的胃炎水平显著降低(P<；0.05)。在胃炎症减轻的同时，幽门螺杆菌感染儿童胃粘膜中Treg细胞数量和Treg细胞因子(转化生长因子[转化生长因子]-β1和白介素10)水平显著高于成人(P<0.05)。此外，儿童幽门螺杆菌感染与胃内转化生长因子-β1和白介素10信使RNA水平显著升高有关。重要的是，幽门螺杆菌感染的儿童胃组织中的转化生长因子-β1主要定位于粘膜CD25(+)和Foxp3(+)细胞，提示转化生长因子-β1的Treg来源。结论：与感染成人相比，幽门螺杆菌感染的儿童胃组织病理改变减轻，局部Treg细胞反应增强，提示胃Treg细胞反应下调了幽门螺杆菌引起的炎症和溃疡。
Background & Aims: Helicobacter pylori infection in children infrequently causes gastroduodenal mucosal ulceration. Because H pylori induces T-cell dependent gastric inflammation in adults and T regulatory (Treg) cells suppress T-cell-dependent pathology, we evaluated gastric histopathology and Treg cell responses in H pylori-infected children and adults. Methods: Gastric tissue from 36 children and 79 adults with abdominal symptoms in Santiago, Chile, was evaluated prospectively for H pylori bacteria and histopathology using the Sydney classification and Treg responses using immunoassay, immunohistochemistry, and real-time polymerase chain reaction. Results: Eighteen (50%) of the children and 51 (65%) of the adults were infected with H pylori. Children and adults were colonized with similar levels of H pylori. However, the level of gastritis in the children was reduced substantially compared with that of the adults (P < .05). Coincident with reduced gastric inflammation, the number of Treg cells and levels of Treg cytokines (transforming growth factor [TGF]-beta 1 and interleukin-10) were increased markedly in the gastric mucosa of H pylori-infected children compared with that of infected adults (P < .03 and < .05, respectively). Also, H pylori infection in the children was associated with markedly increased levels of gastric TGF-beta 1 and interleukin-10 messenger RNA. Importantly, gastric TGF-beta 1 in H pylori-infected children localized predominantly to mucosal CD25(+) and Foxp3(+) cells, indicating a Treg source for the TGF-beta 1. Conclusions: Gastric pathology is reduced and local Treg cell responses are increased in H pylori-infected children compared with infected adults, suggesting that gastric Treg cell responses down-regulate the inflammation and ulceration induced by H pylori in children.