title: Experimental Helicobacter felis infection in transgenic mice expressing human group IIA phospholipase A2.
abstract: BACKGROUND
  Both various virulence factors of Helicobacter pylori and host factors influence the clinical outcome of H. pylori infection. In animal experiments with Helicobacter felis, large variations in the severity of disease have been observed between different mouse strains infected with a single isolate of H. felis. C57BL/6 J mouse strain that lacks the expression of group IIA phospholipase A2 has been shown to develop more severe gastric inflammation than other mouse strains. Thus, group IIA phospholipase A2 has been suggested to play a role in regulating inflammation in gastric mucosa. The aim of this study was to examine the possible role of group IIA phospholipase A2 in experimental Helicobacter infection.
  
  
  METHODS
  Transgenic mice expressing human group IIA phospholipase A2 and their group IIA phospholipase A2 deficient nontransgenic C57BL/6 J littermates were infected with H. felis. The mice were killed 3, 8, and 19 weeks after inoculation of bacteria to determine the histopathological changes in gastric mucosa.
  
  
  RESULTS
  The infected mice developed chronic inflammation in gastric mucosa. We found no differences in the colonization of bacteria between transgenic and nontransgenic mice. At 3 and 8 weeks, no difference was found in the severity of inflammation between the two groups. Nineteen weeks after the administration of bacteria the inflammation was more marked in nontransgenic than transgenic mice. Group IIA phospholipase A2 was expressed by in situ hybridization in the neck cells of the glandular stomach in transgenic mice.
  
  
  CONCLUSIONS
  The results of the present study suggest that the endogenous expression of group IIA phospholipase A2 diminishes chronic inflammation in gastric mucosa in experimental H. felis infection in mice.
authors.affiliation: Department of Surgery, University of Turku and Turku University Central Hospital, Turku, Finland. heikki.huhtinen@fimnet.fi
authors.forename: Heikki T
authors.initials: HT
authors.lastname: Huhtinen
authors.forename: Juha M
authors.initials: JM
authors.lastname: Grönroos
authors.forename: Jaakko
authors.initials: J
authors.lastname: Uksila
authors.forename: David S
authors.initials: DS
authors.lastname: Grass
authors.forename: Timo J
authors.initials: TJ
authors.lastname: Nevalainen
authors.forename: V Jukka O
authors.initials: VJ
authors.lastname: Laine
mesh_terms: D000818:Animals; D030801:Animals, Genetically Modified; D002908:Chronic Disease; D004195:Disease Models, Animal; D005753:Gastric Mucosa / Q000201:enzymology* / Q000382:microbiology / Q000473:pathology; D054501:Group II Phospholipases A2; D016481:Helicobacter Infections / Q000201:enzymology* / Q000382:microbiology / Q000473:pathology; D044922:Helicobacter felis; D017403:In Situ Hybridization; D051379:Mice; D008810:Mice, Inbred C57BL; D010741:Phospholipases A / Q000032:analysis / Q000096:biosynthesis* / Q000097:blood; D054467:Phospholipases A2; D013997:Time Factors
chemical_list: D010741:Phospholipases A; D054501:Group II Phospholipases A2; D054467:Phospholipases A2