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首页> 外文期刊>International journal of medical microbiology: IJMM >Toll-like receptors TLR4, TLR5 and TLR9 on gastric carcinoma cells: An implication for interaction with Helicobacter pylori
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Toll-like receptors TLR4, TLR5 and TLR9 on gastric carcinoma cells: An implication for interaction with Helicobacter pylori

机译：胃癌细胞上的Toll样受体TLR4，TLR5和TLR9：与幽门螺杆菌相互作用的暗示

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In the human stomach Toll-like receptors (TLRs) expressed by the gastric epithelium interact with Helicobacter pylori and mediate production of proinflammatory cytokines and chemokines during H. pylori infection. This results in chronic active gastritis, the background from which gastric carcinoma arises via the epithelial precursor lesions, intestinal metaplasia and dysplasia. Therefore, the question is arising whether gastric carcinoma cells are also able to interact with H. pylori. In this study, TLR4, TLR5 and TLR9 expression was investigated on tumor cells of gastric carcinoma and on its precursor lesions, intestinal metaplasia and dysplasia, by immunohistochemistry. Gastric epithelium with intestinal metaplasia (n = 10) and dysplasia (n = 3) expressed TLR4 and TLR5. TLR4 was strongly expressed by tumor cells of 17 out of 22 and TLR5 by tumor cells of all 22 patients with gastric carcinoma. TLR9, however, was not detectable in intestinal metaplasia or dysplasia, and only focally in 6 out of 22 gastric carcinomas. In contrast to H. pylori gastritis, epithelial TLR expression in intestinal metaplasia, dysplasia and gastric carcinoma was diffusely distributed without subcellular polarization as demonstrated by confocal microscopy. This is the first study describing TLR expression on tumor cells of gastric carcinoma and its precursor lesions. Expression of TLRs enables gastric carcinoma cells to interact with H. pylori. As H. pylori can induce gastric carcinoma-promoting factors, such as IL-8, via epithelial TLR expression, TLR expression by gastric carcinoma cells may have a dangerous potential. (c) 2005 Elsevier GmbH. All rights reserved.
机译：在人胃中，胃上皮细胞表达的Toll样受体（TLR）与幽门螺杆菌相互作用，并在幽门螺杆菌感染期间介导促炎性细胞因子和趋化因子的产生。这导致了慢性活动性胃炎，胃癌通过上皮前体病变，肠上皮化生和异型增生而发生。因此，出现了一个问题，即胃癌细胞是否也能够与幽门螺杆菌相互作用。在这项研究中，通过免疫组织化学研究了TLR4，TLR5和TLR9在胃癌肿瘤细胞及其前体病变，肠上皮化生和发育异常中的表达。肠上皮化生（n = 10）和不典型增生（n = 3）的胃上皮表达TLR4和TLR5。 22例胃癌患者中有22例中有17例肿瘤细胞强烈表达TLR4，22例肿瘤细胞中TLR5强烈表达。然而，在肠上皮化生或异型增生中未检测到TLR9，仅在22个胃癌中有6个是局部检测到的。与幽门螺杆菌胃炎相反，肠上皮化生，异型增生和胃癌中的上皮TLR表达是分散分布的，没有共聚焦显微镜下的亚细胞极化。这是第一项描述TLR在胃癌及其前体病变的肿瘤细胞上表达的研究。 TLR的表达使胃癌细胞能够与幽门螺杆菌相互作用。由于幽门螺杆菌可通过上皮TLR表达诱导胃癌促进因子，例如IL-8，因此胃癌细胞的TLR表达可能具有危险的潜力。 （c）2005 Elsevier GmbH。版权所有。

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