title: [Experimental model of infection of Helicobacter pylori in the mouse. A study of gastric damage caused by indomethacin].
abstract: BACKGROUND
  The action of non-steroidal anti-inflammatory drugs (NSAIDs) on the Helicobacter Pylori (Hp) infected mucosa is a matter of debate. Some authors consider them to cause additive iatrogeny whilst others attribute a purportedly protective action to them. The development of on experimental animal model could help clarify this phenomenon.
  
  
  OBJECTIVE
  1--To develop an animal model of Hp gastric infection. 2--To evaluate the aggressiveness of NSAIDs in this model.
  
  
  METHODS
  Male 6 month old BALC/C mice weighing 38 g were studied. Pylori Hp infection was ruled out. On three occasions, in the same week, 18 mice were inoculated intra-gastrically with 0.6 ml of Hp culture broth (brain-heart infusion) containing 1 x 10 8-1 x 10 9 CFU/ml. Another group of mice were inoculated with sterile saline. After two months the mice were killed and their stomachs studied. They were divided into groups: a) 6 Hp negative control mice. b) 8 Hp negative mice with prior intra-peritoneal injection of 25 mg/Kg indomethacin (24 hs.) c) 8 mice inoculated with Hp with indomethacin. d) 8 mice inoculated with Hp, without indomethacin. The stomachs were opened along the greater curvature and photographed macroscopically in order to map the necrotic area. The antrums were biopsied to test for urease and separate antrum and body specimens were send for staining with Warthin-Starry H & B and histopathology.
  
  
  RESULTS
  All the mice inoculated with Hp acquired the infection. The necrotic area was larger in Group B: 55.5 +/- 7.87 mm than in Group C: 15 +/- 1.82 mm P < 0.00019.
  
  
  RESULTS
  Group A: normal mucosa. Group B: extensive coagulation necrosis and focal erosions. Group C: ulcers with inflammatory infiltrate and smaller necrotic area, presence of Hp on the surface epithelium. Group D: no ulcers, Hp present.
  
  
  CONCLUSIONS
  An animal model of Hp infection was successfully developed Hp infection could play a potentially protective role against indomethacin aggression in the mouse.
authors.affiliation: Servicios de Gastroenterología, Anatomía Patológica, Bacteriología, Hospital Posadas.
authors.forename: M
authors.initials: M
authors.lastname: Schraier
authors.forename: L
authors.initials: L
authors.lastname: Petrelli
authors.forename: M
authors.initials: M
authors.lastname: Bonfanti
authors.forename: A
authors.initials: A
authors.lastname: Di Bella
authors.forename: P
authors.initials: P
authors.lastname: Pest
authors.forename: F
authors.initials: F
authors.lastname: Man
authors.forename: J
authors.initials: J
authors.lastname: Adami
authors.forename: M
authors.initials: M
authors.lastname: Tokumoto
mesh_terms: D000818:Animals; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000009:adverse effects*; D004195:Disease Models, Animal; D005753:Gastric Mucosa / Q000187:drug effects* / Q000382:microbiology / Q000473:pathology; D016481:Helicobacter Infections; D016480:Helicobacter pylori; D007213:Indomethacin / Q000009:adverse effects*; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C
chemical_list: D000894:Anti-Inflammatory Agents, Non-Steroidal; D007213:Indomethacin