title: Helicobacter pylori infection potentiates aspirin induced gastric mucosal injury in Mongolian gerbils.
abstract: BACKGROUND
  Helicobacter pylori infection and non-steroidal anti-inflammatory drugs are two major causes of gastric ulceration but interactions between H pylori and these drugs in gastric mucosal injury are unclear.
  
  
  OBJECTIVE
  We studied the influence of experimental H pylori infection on gastric mucosal injury induced by aspirin.
  
  
  METHODS
  Male Mongolian gerbils free of specific pathogens were used.
  
  
  METHODS
  H pylori ATCC43504 culture broth was administered by oral gavage at seven weeks of age. After three weeks, acidified aspirin (400 mg/kg) was administered orally, and three hours later the total area of gastric erosions, myeloperoxidase (MPO) activity (an index of neutrophil accumulation), thiobarbituric acid reactive substances (TBARS, an index of lipid peroxidation), and KC/GRO (a chemoattractive cytokine in rodents) were measured in gastric mucosa. To determine the role of neutrophils in these circumstances, antigerbil neutrophil rabbit serum (ANS) was administered to some animals 18 hours before aspirin.
  
  
  RESULTS
  Aspirin caused more extensive haemorrhagic erosions (33.1 (12.3) mm2) associated with greater MPO activity (1887.7 (598.5) microU/mg protein) and TBARS (0.33 (0.14) nmol/mg protein) and KC/GRO concentrations (28.3 (9.5) pg/mg protein) in infected than in uninfected gerbils (13.7 (2.3); 204.0 (68.9); 0.12 (0.06); 3.1 (0.8), respectively) Pretreatment with ANS inhibited the increases in gastric erosions, MPO activity, and TBARS but not KC/GRO concentration. The reduction in aspirin induced mucosal injury by administration of ANS was much greater in H pylori infected animals (65%) than in uninfected animals (31%).
  
  
  CONCLUSIONS
  H pylori infection potentiates aspirin induced gastric mucosal injury by mechanisms that include accumulation of activated neutrophils.
authors.affiliation: First Department of Internal Medicine, Kyoto Prefectural University of Medicine, Kyoto 602-8566, Japan. nyoshida@koto.kpu-m.ac.jp
authors.forename: N
authors.initials: N
authors.lastname: Yoshida
authors.forename: N
authors.initials: N
authors.lastname: Sugimoto
authors.forename: F
authors.initials: F
authors.lastname: Hirayama
authors.forename: Y
authors.initials: Y
authors.lastname: Nakamura
authors.forename: H
authors.initials: H
authors.lastname: Ichikawa
authors.forename: Y
authors.initials: Y
authors.lastname: Naito
authors.forename: T
authors.initials: T
authors.lastname: Yoshikawa
mesh_terms: D000818:Animals; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000633:toxicity*; D001241:Aspirin / Q000633:toxicity*; D002630:Chemotactic Factors / Q000032:analysis; D005753:Gastric Mucosa / Q000737:chemistry; D005849:Gerbillinae; D006133:Growth Substances / Q000032:analysis; D016481:Helicobacter Infections / Q000150:complications* / Q000378:metabolism / Q000473:pathology; D016480:Helicobacter pylori; D008297:Male; D020556:Neutrophil Infiltration; D010438:Peptic Ulcer Hemorrhage / Q000209:etiology / Q000378:metabolism / Q000473:pathology; D009195:Peroxidase / Q000378:metabolism; D013276:Stomach Ulcer / Q000209:etiology* / Q000378:metabolism / Q000473:pathology; D017392:Thiobarbituric Acid Reactive Substances / Q000032:analysis
chemical_list: D000894:Anti-Inflammatory Agents, Non-Steroidal; D002630:Chemotactic Factors; D006133:Growth Substances; D017392:Thiobarbituric Acid Reactive Substances; D009195:Peroxidase; D001241:Aspirin