Effect of Helicobacter pylori on gastric epithelial cell migration and proliferation in vitro: Role of VacA and CagA

被引:109
作者
Ricci, V
Ciacci, C
Zarrilli, R
Sommi, P
Tummuru, MKR
Blanco, CD
Bruni, CB
Cover, TL
Blaser, MJ
Romano, M
机构
[1] UNIV NAPLES 2, DIPARTIMENTO INTERNIST CLIN & SPERIMENTALE, CATTEDRA GASTROENTEROL, I-80121 NAPLES, ITALY
[2] UNIV PAVIA, IST FISIOL UMANA, I-27100 PAVIA, ITALY
[3] UNIV NAPLES FEDERICO II, DIPARTIMENTO BIOL PATOL CELLULARE & MOL L CALIFANO, CNR, I-80131 NAPLES, ITALY
[4] VANDERBILT UNIV, SCH MED, DEPT MED, DIV INFECT DIS, NASHVILLE, TN 37232 USA
[5] VET AFFAIRS MED CTR, NASHVILLE, TN 37212 USA
关键词
D O I
10.1128/IAI.64.7.2829-2833.1996
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
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.
引用
收藏
页码:2829 / 2833
页数:5
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