Ricci V, Ciacci C, Zarrilli R, Sommi P, Tummuru M K, Del Vecchio Blanco C, Bruni C B, Cover T L, Blaser M J, Romano M
Istituto di Fisiologia Umana, Università di Pavia, Italy.
Infect Immun. 1996 Jul;64(7):2829-33. doi: 10.1128/iai.64.7.2829-2833.1996.
Helicobacter pylori infection is associated with inflammation of the gastric mucosa and with gastric mucosal damage. In this study, we sought to test the hypothesis that two H. pylori virulence factors (VacA and CagA) impair gastric epithelial cell migration and proliferation, the main processes involved in gastric mucosal healing in vivo. Human gastric epithelial cells (MKN 28) were incubated with undialyzed or dialyzed broth culture filtrates from wild-type H. pylori strains or isogenic mutants defective in production of VacA, CagA, or both products. We found that (i) VacA specifically inhibited cell proliferation without affecting cell migration, (ii) CagA exerted no effect on either cell migration or proliferation, and (iii) undialyzed H. pylori broth culture filtrates inhibited both cell migration and proliferation through a VacA- and CagA-independent mechanism. These findings demonstrate that, in addition to damaging the gastric mucosa, H. pylori products may also impair physiological processes required for mucosal repair.
幽门螺杆菌感染与胃黏膜炎症及胃黏膜损伤有关。在本研究中，我们试图验证以下假设：两种幽门螺杆菌毒力因子（VacA和CagA）会损害胃上皮细胞迁移和增殖，而这是体内胃黏膜愈合的主要过程。将人胃上皮细胞（MKN 28）与野生型幽门螺杆菌菌株或VacA、CagA或两者产物产生缺陷的同基因突变体的未透析或透析肉汤培养滤液一起孵育。我们发现：（i）VacA特异性抑制细胞增殖而不影响细胞迁移；（ii）CagA对细胞迁移或增殖均无影响；（iii）未透析的幽门螺杆菌肉汤培养滤液通过一种不依赖VacA和CagA的机制抑制细胞迁移和增殖。这些发现表明，除了损害胃黏膜外，幽门螺杆菌产物还可能损害黏膜修复所需的生理过程。
