Duodenogastric reflux and Helicobacter pylori infection synergistically increase gastric mucosal cell proliferative activity in mongolian gerbils

Background: Helicobacterpylori and duodenogastric reflux (DGR) are both recognized as actiological factors in chronic gastritis and gastric carcinogenesis. In this study, a Mongolian gerbil (Mg) model was used to investigate the histopathological changes in the gastric mucosa resulting fron DGR and/or H. pylori infection. Methods: One-hundred-and-eleven 7-week-old. specific-pathogen-free. male MGs were divided into four groups: normal controls, gerbils with surgically induced DGR, and H. pylori-infected gerbils with and without DGR. Gerbils were killed 4, 12 and 26 weeks after DGR surgery their stomachs removed and sections prepared. Sections were fixed immediately in 20% phosphate-buffered formalin and subjected to haematoxlin and eosin staining. Alcian blue at pH 2.5 periodic acid-Schiff staining, and immunostaining for smooth muscle cells, H. pylori and 5'-bronio-2'-deoxyuridine (BrdU). Results: The gastric mucosa of H. pylori-infected gerbils showed chronic active gastritis irrespective of DGR throughout the experimental period. The gastric mucosa of H. pylori-infectedgerbils with DGR demonstrated higher BrdU labelling than in the other group;. Conclusions: In MGs. DGR and H. pylori infection synergistically increased gastric mucosal cell proliferative activity. DGR and H.pylori infection may be involved synergistically in gastric carcinogenesis by increasing cell proliferative activity.