Helicobacter pylori culture supernatant inhibits binding and proliferative response of human gastric cells to epidermal growth factor: implications for H.pylori interference with ulcer healing?
Helicobacter pylori culture supernatant inhibits binding and proliferative response of human gastric cells to epidermal growth factor: implications for H.pylori interference with ulcer healing?
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幽门螺杆菌培养上清液抑制人胃细胞对表皮生长因子的结合和增殖反应：幽门螺杆菌干扰溃疡愈合的影响？
DOI：
10.1159/000201458
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发表时间：
1997
期刊：
影响因子：
3.2
通讯作者：
A. Tarnawski
中科院分区：
文献类型：
--
作者：
Y. Fujiwara;F. Wyle;T. Arakawa;M. Domek;T. Fukuda;Kenzo Kobayashi;A. Tarnawski
幽门螺杆菌（H.幽门螺杆菌）感染与胃炎和消化性溃疡病密切相关。然而，H. pylori和/或H.幽门螺杆菌与溃疡愈合的关系尚不清楚。表皮生长因子（EGF）通过与其受体结合，加速细胞迁移并触发上皮细胞增殖，这两者对胃十二指肠溃疡的愈合都很重要。H.幽门螺杆菌似乎干扰溃疡愈合，但这些作用的细胞和分子靶点和机制尚未阐明。在本研究中，我们测试了H. pylori培养上清液（透析以除去小于10 kD的分子）对EGF与其受体结合的影响以及对人胃Kato III细胞对EGF的增殖反应的影响。H. pylori培养上清显著降低EGF与其受体的特异性结合，并降低EGF刺激的胃细胞增殖。由于溃疡愈合需要上皮细胞增殖和细胞迁移（再上皮化），这两者都是由EGF与其受体结合触发的，因此H. pylori产物可能是H.幽门引起的对溃疡愈合的干扰。
Helicobacter pylori (H. pylori) infection of gastric mucosa is strongly associated with gastritis and peptic ulcer disease. However, the mechanisms of the ulcerogenic action of H. pylori and/or the interference of H. pylori with ulcer healing are unknown. Through binding to its receptor, epidermal growth factor (EGF) accelerates cells migration and triggers epithelial cell proliferation which are both important for the healing of gastroduodenal ulcers. H. pylori seems to interfere with ulcer healing, but the cellular and molecular targets and mechanisms of these actions have not been elucidated. In the present study, we tested the effect of H. pylori culture supernatant (dialyzed to remove molecules smaller than 10 kD) on EGF binding to its receptor and on the proliferative response of human gastric Kato III cells to EGF. H. pylori culture supernatant significantly reduced specific binding of EGF to its receptor and reduced EGF-stimulated gastric cell proliferation. Since ulcer healing requires epithelial cell proliferation and cell migration (re-epithelialization), which are both triggered by EGF binding to its receptor, the alteration in these mechanisms by H. pylori product may be the basis of H. pylori-induced interference with ulcer healing.