Helicobacter pylori infection stimulates intestinalization of endocrine cells in glandular stomach of Mongolian gerbils

Yoshiharu Takenaka, Tetsuya Tsukamoto, Tsutomu Mizoshita, Xueyuan Cao, Hisayo Ban, Naotaka Ogasawara, Michio Kaminishi, Masae Tatematsu

Research output: Contribution to journalArticle

6 Citations (Scopus)

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.

Original languageEnglish
Pages (from-to)1015-1022
Number of pages8
JournalCancer science
Volume97
Issue number10
DOIs
Publication statusPublished - 10-2006

All Science Journal Classification (ASJC) codes

  • Oncology
  • Cancer Research

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