title: Association of cytotoxin production and neutrophil activation by strains of Helicobacter pylori isolated from patients with peptic ulceration and chronic gastritis.
abstract: BACKGROUND
  Helicobacter pylori is associated with neutrophil infiltration within the gastroduodenal mucosa. Neutrophil activation provides a major source of oxygen free radicals, which have been implicated in the pathogenesis of peptic ulceration.
  
  
  OBJECTIVE
  To investigate if cytotoxin producing strains of H pylori are associated with the generation of oxidative burst in polymorphonuclear neutrophils (PMNs).
  
  
  METHODS
  76 patients undergoing endoscopy of whom 45 had peptic ulcer and 31 chronic gastritis only were studied.
  
  
  METHODS
  Strains of H pylori were cultured in Brucella broth. After 48 hours, bacteria were harvested by centrifugation and a bacterial suspension prepared as a stimulus for PMN oxidative burst using chemiluminescence. PMNs were prepared from health blood donors. To test the ability of strains to produce cytotoxin, culture supernatants of each were concentrated by polyethylene glycol and tested on cultured Vero cells for intracellular vacuolation.
  
  
  RESULTS
  30 of 45 (66.7%) peptic ulcer patients induced cell vacuolation versus nine of 31 (29%) strains from patients with chronic gastritis only (p < 0.01). Cytotoxin positive strains of H pylori regardless of the presence or absence of peptic ulcer displayed an increased induction of respiratory burst in PMNs compared with toxin negative strains from patients with chronic gastritis only (p < 0.05). Among the toxin negative strains, those from patients with peptic ulcer did not show a significant increase of the oxidative burst than those from patients without peptic ulcer (NS).
  
  
  CONCLUSIONS
  Toxinogenicity of strains of H pylori seems to be correlated with neutrophil respiratory burst and peptic ulceration. The ability of some strains of H pylori to produce cytotoxin and to induce the oxidative burst in neutrophils may be important in the pathogenesis of peptic ulcer disease.
authors.affiliation: Department of Gastroenterology, University of Glasgow NHS Trust.
authors.forename: Q B
authors.initials: QB
authors.lastname: Zhang
authors.forename: I M
authors.initials: IM
authors.lastname: Nakashabendi
authors.forename: M S
authors.initials: MS
authors.lastname: Mokhashi
authors.forename: J B
authors.initials: JB
authors.lastname: Dawodu
authors.forename: C G
authors.initials: CG
authors.lastname: Gemmell
authors.forename: R I
authors.initials: RI
authors.lastname: Russell
mesh_terms: D000328:Adult; D000368:Aged; D000818:Animals; D002478:Cells, Cultured; D002522:Chlorocebus aethiops; D002908:Chronic Disease; D003603:Cytotoxins / Q000096:biosynthesis*; D005260:Female; D005756:Gastritis / Q000378:metabolism; D016480:Helicobacter pylori / Q000302:isolation & purification / Q000378:metabolism*; D006801:Humans; D008163:Luminescent Measurements; D008297:Male; D008875:Middle Aged; D009504:Neutrophils / Q000378:metabolism*; D017382:Reactive Oxygen Species / Q000378:metabolism; D016897:Respiratory Burst / Q000187:drug effects*; D013276:Stomach Ulcer / Q000378:metabolism*; D014709:Vero Cells
chemical_list: D003603:Cytotoxins; D017382:Reactive Oxygen Species