title: Influence of COX-2 and local cytokine expressions in gastric ulcer mucosa by H. pylori and NSAID.
abstract: OBJECTIVE
  H. pylori and NSAIDs are the two most important pathogenic factors in gastric ulcer. NSAIDs and H. pylori share common pathogenic characteristics, but have different effects in modulating COX-2 and local cytokines in gastric ulcer mucosa. This study was designed to explore the influence of COX-2 and local cytokine expressions in gastric ulcer mucosa induced by H. pylori infection and NSAID use.
  
  
  METHODS
  Twenty-three patients were recruited. Sixteen subjects were infected with H. pylori. Fifteen patients used NSAIDs. Gastric biopsy specimens were obtained by endoscopy. COX-2 and local cytokine mRNA expressions were assessed by real-time RT-PCR.
  
  
  RESULTS
  COX-2 and local cytokines were over-expressed in gastric ulcer and were positively intercorrelated. H. pylori did not alter COX-2 and local cytokine expressions in gastric ulcer, but induced IL-8 and COX-2 in antral mucosa. NSAIDs inhibited COX-2 expression in gastric ulcer, but had no effect on other local cytokines. COX-2 inhibition by NSAIDs in gastric ulcer was compatible with the findings that NSAIDs delayed gastric ulcer healing.
  
  
  CONCLUSIONS
  H. pylori increased IL-8 and COX-2 in the antral mucosa, but did not influence COX-2 and local cytokines in gastric ulcer. NSAIDs inhibited COX-2 in gastric ulcer and delayed gastric ulcer healing.
authors.affiliation: Graduate Institute of Clinical Medicine, College of Medicine, National Taiwan University, Taipei.
authors.forename: Chun-Ying
authors.initials: CY
authors.lastname: Wu
authors.forename: Ming-Shing
authors.initials: MS
authors.lastname: Wu
authors.forename: Yi-Ju
authors.initials: YJ
authors.lastname: Chen
authors.forename: Chien-Jen
authors.initials: CJ
authors.lastname: Chen
authors.forename: Jaw-Town
authors.initials: JT
authors.lastname: Lin
authors.forename: Gran-Hum
authors.initials: GH
authors.lastname: Chen
mesh_terms: D000328:Adult; D000368:Aged; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000378:metabolism*; D051546:Cyclooxygenase 2 / Q000378:metabolism*; D016099:Endoscopy, Gastrointestinal; D005260:Female; D016480:Helicobacter pylori; D006801:Humans; D015847:Interleukin-4 / Q000378:metabolism; D016209:Interleukin-8 / Q000378:metabolism*; D007413:Intestinal Mucosa / Q000378:metabolism*; D008297:Male; D008565:Membrane Proteins / Q000378:metabolism*; D008875:Middle Aged; D011446:Prospective Studies; D011706:Pyloric Antrum / Q000378:metabolism; D020133:Reverse Transcriptase Polymerase Chain Reaction; D013276:Stomach Ulcer / Q000188:drug therapy / Q000378:metabolism* / Q000503:physiopathology; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism; D014945:Wound Healing
chemical_list: D000894:Anti-Inflammatory Agents, Non-Steroidal; D016209:Interleukin-8; D008565:Membrane Proteins; D014409:Tumor Necrosis Factor-alpha; D015847:Interleukin-4; D051546:Cyclooxygenase 2; C496540:PTGS2 protein, human