Upregulation of CCL20 and recruitment of CCR6+ gastric infiltrating lymphocytes in Helicobacter pylori gastritis
Upregulation of CCL20 and recruitment of CCR6+ gastric infiltrating lymphocytes in Helicobacter pylori gastritis
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DOI：
10.1128/iai.01660-06
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发表时间：
2007-09-01
影响因子：
3.1
通讯作者：
Hsu, Ping-Ning
中科院分区：
文献类型：
--
作者：
Wu, Yi-Ying;Tsai, Hwei-Fang;Hsu, Ping-Ning
幽门螺杆菌感染与胃粘膜的炎症反应有关，导致慢性胃炎、消化性溃疡和胃癌。H感染部位T细胞浸润增加。幽门。CCR 6是CCL 20（MIP-3 alpha/LARC/exodus）的特异性β-趋化因子受体，近年来研究发现CCR 6可介导胃粘膜组织中淋巴细胞的稳态和免疫应答，并可能在胃炎症过程中参与趋化因子介导的淋巴细胞运输。在这项研究中，我们研究了CCR 6及其配体CCL 20在H.幽门感染从H. pylori胃炎患者中，并分析CCR 6趋化因子受体的表达。我们的研究结果表明，在浸润胃粘膜的CD 3（+）T细胞中，CCR 6的表达显著增加，CCR 6配体（CCL 20趋化因子）选择性地在炎症胃组织中表达。CCL 20的产生在H. pylori在胃上皮细胞中的表达，当有促炎细胞因子白细胞介素-1 β和肿瘤坏死因子α刺激时。此外，重组CCL 20诱导淋巴细胞趋化性迁移在新鲜的胃T细胞离体，表明胃T细胞可以通过CCR 6/CCL 20相互作用向炎症部位迁移。我们的研究结果表明，CCL 20和CCR 6之间的相互作用可能在趋化因子介导的淋巴细胞运输过程中发挥作用，在胃炎症螺杆菌感染。
Helicobacter pylori infection is associated with an inflammatory response in the gastric mucosa, leading to chronic gastritis, peptic ulcers, and gastric cancer. There is increased T-cell infiltration at the site of infection with H. pylori. CCR6, a specific beta-chemokine receptor for CCL20 (MIP-3 alpha/LARC/exodus), has recently been reported to mediate lymphocyte homeostasis and immune responses in mucosal tissue, and it may play a role in chemokine-mediated lymphocyte trafficking during gastric inflammation. In this study, we investigated the role of CCR6 and its ligand, CCL20, in inducing an inflammatory response in the gastric mucosa during H. pylori infection. Gastric infiltrating T lymphocytes were isolated from endoscopic biopsy specimens of H. pylori gastritis patients and analyzed for the expression of the CCR6 chemokine receptor. Our results demonstrated that there was significantly increased CCR6 expression in CD3(+) T cells infiltrating the gastric mucosa, and the CCR6 ligand, the CCL20 chemokine, was selectively expressed in inflamed gastric tissues. The production of CCL20 was upregulated in response to H. pylori in gastric epithelial cells when there was stimulation by the proinflammatory cytokines interleukin-1 beta and tumor necrosis factor alpha. Furthermore, recombinant CCL20 induced lymphocyte chemotaxis migration in fresh gastric T cells ex vivo, indicating that the gastric T cells could migrate toward inflammatory sites via CCR6/CCL20 interaction. Our results suggest that the interaction between CCL20 and CCR6 may play a role in chemokine-mediated lymphocyte trafficking during gastric inflammation in Helicobacter infection.