title: Effects of Helicobacter pylori infection on the link between regenerating gene expression and serum gastrin levels in Mongolian gerbils.
abstract: 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.
authors.affiliation: Department of Pathology, Medicine, Veterans Affairs Medical Center and Baylor College of Medicine, Houston, Texas, USA.
authors.forename: Hirokazu
authors.initials: H
authors.lastname: Fukui
authors.forename: Francesco
authors.initials: F
authors.lastname: Franceschi
authors.forename: Rebecca L
authors.initials: RL
authors.lastname: Penland
authors.forename: Taro
authors.initials: T
authors.lastname: Sakai
authors.forename: Antonia R
authors.initials: AR
authors.lastname: Sepulveda
authors.forename: Takahiro
authors.initials: T
authors.lastname: Fujimori
authors.forename: Akira
authors.initials: A
authors.lastname: Terano
authors.forename: Tsutomu
authors.initials: T
authors.lastname: Chiba
authors.forename: Robert M
authors.initials: RM
authors.lastname: Genta
mesh_terms: D000818:Animals; D000900:Anti-Bacterial Agents / Q000627:therapeutic use; D017209:Apoptosis; D001483:Base Sequence; D002135:Calcium-Binding Proteins / Q000235:genetics / Q000378:metabolism*; D002455:Cell Division; D004195:Disease Models, Animal; D005745:Gastric Acidity Determination; D005753:Gastric Mucosa / Q000473:pathology; D005755:Gastrins / Q000097:blood*; D005756:Gastritis / Q000188:drug therapy / Q000378:metabolism / Q000473:pathology; D005849:Gerbillinae; D016481:Helicobacter Infections / Q000188:drug therapy / Q000378:metabolism* / Q000473:pathology; D016480:Helicobacter pylori / Q000187:drug effects / Q000302:isolation & purification / Q000472:pathogenicity*; D051847:Lithostathine; D008297:Male; D008969:Molecular Sequence Data; D009419:Nerve Tissue Proteins; D012333:RNA, Messenger / Q000378:metabolism; D016415:Sequence Alignment; D015854:Up-Regulation
chemical_list: D000900:Anti-Bacterial Agents; D002135:Calcium-Binding Proteins; D005755:Gastrins; D051847:Lithostathine; D009419:Nerve Tissue Proteins; D012333:RNA, Messenger