Fujiwara Y, Wyle F, Arakawa T, Domek M J, Fukuda T, Kobayashi K, Tarnawski A
Department of Veterans Affairs Medical Center, Long Beach, CA 90822, USA.
Digestion. 1997;58(3):299-303. doi: 10.1159/000201458.
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.
胃黏膜幽门螺杆菌（H. pylori）感染与胃炎和消化性溃疡病密切相关。然而，幽门螺杆菌致溃疡作用的机制和/或幽门螺杆菌对溃疡愈合的干扰尚不清楚。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。幽门螺杆菌似乎会干扰溃疡愈合，但这些作用的细胞和分子靶点及机制尚未阐明。在本研究中，我们测试了幽门螺杆菌培养上清液（经透析以去除小于10 kD的分子）对EGF与其受体结合以及对人胃Kato III细胞对EGF增殖反应的影响。幽门螺杆菌培养上清液显著降低了EGF与其受体的特异性结合，并降低了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（重新上皮化），而这两者均由EGF与其受体结合触发，因此幽门螺杆菌产物对这些机制的改变可能是幽门螺杆菌诱导干扰溃疡愈合的基础。
