title: Long-term evaluation of mice model infected with Helicobacter pylori: focus on gastric pathology including gastric cancer.
abstract: BACKGROUND
  Long-term evaluation of gastric pathology after H. pylori infection is very important in order to reveal its clinical implications, since debate still exists on the gastric carcinogenesis provoked by H. pylori infection in animal models.
  
  
  OBJECTIVE
  Either to evaluate the long-term outcome of H. pylori infection or to determine how H. pylori could provoke gastric cancer in the mice model.
  
  
  METHODS
  Four-week-old specific pathogen free C57BL/6 mice (n = 115) were infected with SS1, the mouse-adapted H. pylori strain. After 4, 8, 16, 24, 36, 50 and 80 weeks of bacterial infection, the H. pylori-infected mice were sacrificed.
  
  
  RESULTS
  After 80 weeks of infection, almost all the H. pylori-infected mice developed hyperplastic gastritis, but did not show any evidence of gastric adenoma, dysplasia or carcinoma. PCNA positive cells were most abundant after 50 weeks and tended to decrease thereafter up to 80 weeks, whereas apoptosis began to be noted 8 weeks after H. pylori infection, showing 7-8 apoptotic cells/high power field, and tending to increase as time passed. Normally observed neutral mucin decreased during the experiment, showing the most marked decrease 50 weeks after H. pylori infection. In contrast, acidic mucin was noted from 50 weeks after infection.
  
  
  CONCLUSIONS
  The SS1-infected mouse seems to be a suitable animal model for H. pylori-related research, and H. pylori itself does not induce gastric cancer in normal wild-type mouse model following long-term exposure, which could be explained by the balance that exists between cell proliferation and apoptosis.
authors.affiliation: Genomic Research Center for Gastroenterology and Ajou Helicobacter pylori Research Group, Ajou University School of Medicine, Suwon, Korea.
authors.forename: D H
authors.initials: DH
authors.lastname: Kim
authors.forename: S W
authors.initials: SW
authors.lastname: Kim
authors.forename: Y J
authors.initials: YJ
authors.lastname: Song
authors.forename: T Y
authors.initials: TY
authors.lastname: Oh
authors.forename: S U
authors.initials: SU
authors.lastname: Han
authors.forename: Y B
authors.initials: YB
authors.lastname: Kim
authors.forename: H J
authors.initials: HJ
authors.lastname: Joo
authors.forename: Y K
authors.initials: YK
authors.lastname: Cho
authors.forename: D Y
authors.initials: DY
authors.lastname: Kim
authors.forename: S W
authors.initials: SW
authors.lastname: Cho
authors.forename: M W
authors.initials: MW
authors.lastname: Kim
authors.forename: J H
authors.initials: JH
authors.lastname: Kim
authors.forename: K B
authors.initials: KB
authors.lastname: Hahm
mesh_terms: D000818:Animals; D017209:Apoptosis; D005756:Gastritis / Q000382:microbiology*; D016481:Helicobacter Infections / Q000150:complications* / Q000473:pathology; D016480:Helicobacter pylori; D007150:Immunohistochemistry; D020287:In Situ Nick-End Labeling; D051379:Mice; D008810:Mice, Inbred C57BL; D008954:Models, Biological; D009077:Mucins / Q000378:metabolism; D018809:Proliferating Cell Nuclear Antigen / Q000378:metabolism; D013274:Stomach Neoplasms / Q000382:microbiology*
chemical_list: D009077:Mucins; D018809:Proliferating Cell Nuclear Antigen