Although regenerating gene (Reg)
protein is reported to have a trophic effect on gastric epithelial cells, its involvement in human
gastric diseases is not clear. We have recently shown that both
gastrin and gastric mucosal
inflammation enhance Reg gene expression in the fundic mucosa in rats. This study was designed to clarify whether Reg
protein is involved in Helicobacter pylori-induced
gastritis and whether Reg gene expression is linked to serum
gastrin levels in this condition. Mongolian gerbils were inoculated with an H. pylori strain isolated from a
gastric cancer patient. Four weeks later, some of the gerbils with H. pylori
infection were eradicated by
lansoprazole,
amoxicillin, and
clarithromycin. The time courses of changes in Reg gene expression, serum
gastrin levels, gastric acidity, and histopathologic factors were examined. Four weeks after H. pylori
infection,
gastritis started spreading to the fundic mucosa, and gastric acidity started reducing. Serum
gastrin levels and Reg
mRNA expression in the fundus were significantly increased 6 weeks after
infection. Reg
mRNA expression in the fundus correlated significantly with both serum
gastrin levels and the severity of fundic mucosal
inflammation. After H. pylori eradication, serum
gastrin levels and fundic mucosal
inflammation were normalized, and the increase in Reg
mRNA expression was abolished. The Reg gene is associated with hypergastrinemia and fundic mucosal
inflammation and may be involved in H. pylori-induced
gastritis.