Inflammatory cells in the gastric epithelium and direct cell damage are imp
ortant effects of H. pylori infection in causing gastroduodenal diseases. T
he aim of this study was to determine whether H. Pylori possessing the cagA
gene and vacuolating cytotoxin activity (cagA +/tox+) has these toxigenici
ties. The detection of cagA was performed by the polymerase chain reaction
method. Culture supernatants of H. pylori were tested on rabbit gastric epi
thelial cell culture for intracellular vacuolation. H. pylori isolates were
divided into two major types, cagA +/tox+ and cagA -/tox- strains. Ten Jap
anese monkeys were allocated to two groups, with six animals inoculated wit
h the cagA+/tox+ strain and four animals inoculated with the cagA-/tox- str
ain. Five other Japanese monkeys served as controls. They were observed end
oscopically every week and the severity of gastritis was evaluated in biops
y specimens obtained from the antral mucosa. Histopathological examination
of the gastric mucosa revealed a more severe neutrophil infiltration caused
by the cagA+/tox+ strain than that caused by the cagA-/tox- strain for 3 m
onths after inoculation. These findings indicate that cagA and vacuolating
cytotoxin may be important factors in causing the severe damage of the huma
n gastric mucosa produced by H. pylori.