title: Inducible nitric oxide synthase expression in gastroduodenal diseases infected with Helicobacter pylori.
abstract: BACKGROUND
  Nitric oxide (NO) is synthesized enzymatically from L-arginine by NO synthase, which is measured by inducible NO synthase (iNOS). Helicobacter pylori (H. pylori) infection produces a state of chronic immunostimulation in the gastric epithelium. Infection with cagA+ H. pylori has greater degree of gastric inflammation and epithelial cell damage. Therefore, we compared the levels of iNOS in patients with H. pylori infection in relation to cagA status and H. pylori-related disease.
  
  
  METHODS
  One hundred and seven patients, including 51 patients with gastric cancer, 12 patients with gastric ulcer, 18 patients with duodenal ulcer and 26 patients with chronic gastritis, were enrolled in this study. Biopsies from the antrum and body were obtained for histologic examination, culture and reverse transcriptionase-PCR (RT-PCR) for detection of iNOS gene expression. The presence of H. pylori was confirmed by Giemsa staining or culture and the gene expression of cagA in H. pylori isolates was confirmed by PCR.
  
  
  RESULTS
  H. pylori infection was detected in 70.1% (75/107) and cagA was detected in 84.8% (28/33). iNOS expression was detected in 49.5% (53/107) and there was no significant difference in iNOS expression according to H. pylori infection nor the cagA status in the gastroduodenal diseases. However, iNOS expression was more frequently detected in gastric cancer than the other H. pylori-related diseases (64.7% vs. 35.7%, p <.05).
  
  
  CONCLUSIONS
  Although NO was thought be involved in the gastric carcinogenesis, the level of NO production was not related to H. pylori infection or cagA status.
authors.affiliation: Department of Medicine, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Korea.
authors.forename: H J
authors.initials: HJ
authors.lastname: Son
authors.forename: J C
authors.initials: JC
authors.lastname: Rhee
authors.forename: D I
authors.initials: DI
authors.lastname: Park
authors.forename: Y H
authors.initials: YH
authors.lastname: Kim
authors.forename: P L
authors.initials: PL
authors.lastname: Rhee
authors.forename: K C
authors.initials: KC
authors.lastname: Koh
authors.forename: S W
authors.initials: SW
authors.lastname: Paik
authors.forename: K W
authors.initials: KW
authors.lastname: Choi
authors.forename: J J
authors.initials: JJ
authors.lastname: Kim
mesh_terms: D000328:Adult; D000368:Aged; D000942:Antigens, Bacterial; D001426:Bacterial Proteins / Q000378:metabolism; D002908:Chronic Disease; D004269:DNA, Bacterial / Q000032:analysis; D004381:Duodenal Ulcer / Q000201:enzymology* / Q000382:microbiology / Q000473:pathology; D005260:Female; D005753:Gastric Mucosa / Q000201:enzymology / Q000473:pathology; D005756:Gastritis / Q000201:enzymology* / Q000382:microbiology / Q000473:pathology; D016481:Helicobacter Infections / Q000378:metabolism* / Q000382:microbiology / Q000473:pathology; D016480:Helicobacter pylori; D006801:Humans; D008297:Male; D008875:Middle Aged; D019001:Nitric Oxide Synthase / Q000378:metabolism*; D052247:Nitric Oxide Synthase Type II; D011706:Pyloric Antrum / Q000201:enzymology / Q000473:pathology; D020133:Reverse Transcriptase Polymerase Chain Reaction; D013274:Stomach Neoplasms / Q000201:enzymology* / Q000382:microbiology / Q000473:pathology; D013276:Stomach Ulcer / Q000201:enzymology* / Q000382:microbiology / Q000473:pathology
chemical_list: D000942:Antigens, Bacterial; D001426:Bacterial Proteins; D004269:DNA, Bacterial; C080866:cagA protein, Helicobacter pylori; C496319:NOS2 protein, human; D019001:Nitric Oxide Synthase; D052247:Nitric Oxide Synthase Type II