title: Mechanism of action of low recurrence of gastritis caused by Helicobacter pylori with the type II urease B gene.
abstract: BACKGROUND
  Low recurrence of gastritis is seen in patients infected with Helicobacter pylori carrying the type II urease B gene, compared with H. pylori carrying types I and III. The underlying mechanism has been studied in terms of the urease activity and interleukin (IL)-8 production capacity of different strains of H. pylori.
  
  
  METHODS
  Forty-five patients infected with different strains of H. pylori (type I; 15, type II; 15 and type III; 15) were enrolled in the study. H. pylori was isolated from gastric mucosa and cultured in the presence of urea at pH 5.5 to evaluate urease activity. The capacity of different strains of H. pylori to induce IL-8 mRNA and IL-8 from a human gastric cancer cell line and human peripheral blood mononuclear cells was evaluated.
  
  
  RESULTS
  The urease activity of type II H. pylori[523 +/- 228 micro g of ammonia/dl/10(8) colony-forming units (CFU)/ml] was significantly lower than that of type I (1355 +/- 1369 micro g of ammonia/dl/10(8) CFU/ml) and type III (1442 +/- 2229 micro g of ammonia/dl/10(8) CFU/ml) (p <.05). Gastric cancer cells cocultured with type II H. pylori produced lower levels of IL-8 mRNA compared with type I and type III H. pylori. The levels of IL-8 were also significantly lower in cultures induced by type II H. pylori compared with those induced by type I and type III H. pylori. Peripheral blood mononuclear cells also produced lower levels of IL-8 when cocultured with type II compared with type I H. pylori.
  
  
  CONCLUSIONS
  These results indicate that both the lower level of urease activity and the low IL-8-inducing capacity of type II H. pylori might underlie the lower recurrence rate of gastritis caused by type II H. pylori.
authors.affiliation: Third Department of Internal Medicine, Ehime University School of Medicine, Ehime, Japan.
authors.forename: Md
authors.initials: M
authors.lastname: Badruzzaman
authors.forename: Hidetaka
authors.initials: H
authors.lastname: Matsui
authors.forename: Sk Md
authors.initials: SM
authors.lastname: Fazle Akbar
authors.forename: Bunzo
authors.initials: B
authors.lastname: Matsuura
authors.forename: Morikazu
authors.initials: M
authors.lastname: Onji
mesh_terms: D000942:Antigens, Bacterial / Q000235:genetics; D001426:Bacterial Proteins / Q000235:genetics; D002460:Cell Line; D016172:DNA Fingerprinting; D004269:DNA, Bacterial / Q000032:analysis / Q000302:isolation & purification; D005260:Female; D005756:Gastritis / Q000382:microbiology* / Q000503:physiopathology; D015870:Gene Expression; D005838:Genotype; D016481:Helicobacter Infections / Q000382:microbiology* / Q000503:physiopathology*; D016480:Helicobacter pylori / Q000201:enzymology* / Q000235:genetics* / Q000302:isolation & purification / Q000472:pathogenicity; D006801:Humans; D016209:Interleukin-8 / Q000096:biosynthesis; D007963:Leukocytes, Mononuclear / Q000276:immunology; D008297:Male; D008875:Middle Aged; D016133:Polymerase Chain Reaction; D012150:Polymorphism, Restriction Fragment Length; D012333:RNA, Messenger / Q000032:analysis / Q000302:isolation & purification; D012008:Recurrence; D013274:Stomach Neoplasms; D014510:Urease / Q000235:genetics* / Q000378:metabolism
chemical_list: D000942:Antigens, Bacterial; D001426:Bacterial Proteins; D004269:DNA, Bacterial; D016209:Interleukin-8; D012333:RNA, Messenger; C080866:cagA protein, Helicobacter pylori; D014510:Urease