title: Helicobacter pylori infection stimulates intestinalization of endocrine cells in glandular stomach of Mongolian gerbils.
abstract: Intestinal metaplasia has been investigated extensively as a possible premalignant condition for stomach cancer but its pathogenesis is still not fully understood. In the present study, we examined the relationship between endocrine and mucous cell marker expression periodically after Helicobacter pylori infection in the Mongolian gerbil model. The numbers of chromogranin A (CgA)-positive, gastrin-positive and gastric inhibitory polypeptide (GIP)-positive cells in H. pylori-infected groups was increased significantly compared with the non-infected case. However, CgA-positive and gastrin-positive cells then decreased from 50 through 100 experimental weeks after H. pylori infection, whereas GIP-positive cells increased. Coexistence of gastrin-positive and GIP-positive cells was detected in the same gastric and intestinal mixed phenotypic glandular-type glands. In conclusion, the endocrine cell phenotype is in line with that of the mucous counterpart in the glands of H. pylori-infected Mongolian gerbil stomach, supporting the concept that development of intestinal metaplasia is due to the abnormal differentiation of a stem cell.
authors.affiliation: Division of Oncological Pathology, Aichi Cancer Center Research Institute, 1-1 Kanokoden, Chikusa, Nagoya, Japan.
authors.forename: Yoshiharu
authors.initials: Y
authors.lastname: Takenaka
authors.forename: Tetsuya
authors.initials: T
authors.lastname: Tsukamoto
authors.forename: Tsutomu
authors.initials: T
authors.lastname: Mizoshita
authors.forename: Xueyuan
authors.initials: X
authors.lastname: Cao
authors.forename: Hisayo
authors.initials: H
authors.lastname: Ban
authors.forename: Naotaka
authors.initials: N
authors.lastname: Ogasawara
authors.forename: Michio
authors.initials: M
authors.lastname: Kaminishi
authors.forename: Masae
authors.initials: M
authors.lastname: Tatematsu
mesh_terms: D000818:Animals; D053379:Chromogranin A; D002864:Chromogranins / Q000032:analysis / Q000235:genetics; D004702:Endocrine Glands / Q000737:chemistry / Q000473:pathology; D005749:Gastric Inhibitory Polypeptide / Q000032:analysis / Q000235:genetics; D005753:Gastric Mucosa / Q000737:chemistry / Q000473:pathology; D005755:Gastrins / Q000032:analysis / Q000235:genetics; D005849:Gerbillinae; D016481:Helicobacter Infections / Q000150:complications*; D016480:Helicobacter pylori; D007150:Immunohistochemistry; D007422:Intestines / Q000473:pathology*; D008679:Metaplasia; D011230:Precancerous Conditions / Q000473:pathology*; D012333:RNA, Messenger / Q000032:analysis; D013270:Stomach / Q000737:chemistry / Q000382:microbiology* / Q000473:pathology*; D013274:Stomach Neoplasms / Q000473:pathology*
chemical_list: D053379:Chromogranin A; D002864:Chromogranins; D005755:Gastrins; D012333:RNA, Messenger; D005749:Gastric Inhibitory Polypeptide