title: Increased expression of IL-10 and IL-12 (p40) mRNA in Helicobacter pylori infected gastric mucosa: relation to bacterial cag status and peptic ulceration.
abstract: OBJECTIVE
  To investigate interleukin (IL)-12 (p40) and IL-10 mRNA expression levels in the gastric mucosa in relation to H pylori cag status, peptic ulceration, and histopathology.
  
  
  METHODS
  In 81 dyspeptic patients, antral and corpus biopsies were taken for reverse transcriptase polymerase chain reaction (RT-PCR) and histology. G3PDH (control) and IL-10 and IL-12 were coamplified in a duplex PCR and the ratios of cytokines to G3PDH were determined. Bacterial ureA and cagA status was determined by RT-PCR.
  
  
  RESULTS
  IL-10 mRNA expression in both the antral and corpus mucosa was greater (p < 0.01) in cagA positive infection than in H pylori negative patients with histologically normal mucosa. No increase in IL-10 mRNA expression was observed in cagA negative infection. Both in the antral and corpus mucosa, IL-12 mRNA expression was greater (p < 0.05) in cagA positive than in cagA negative infection and uninfected patients with normal gastric mucosa. In cagA positive infection, there was a correlation between IL-10 and IL-12 mRNA expression in both the antral mucosa (r = 0.515, p < 0.01) and the corpus mucosa (r = 0.6, p < 0.005). IL-12 mRNA expression in the antral mucosa was significantly more frequent in H pylori positive patients with duodenal ulcer than in those with gastric ulcer or nonulcer dyspepsia. No difference was observed in IL-10 mRNA expression in relation to endoscopic diagnosis.
  
  
  CONCLUSIONS
  CagA positive H pylori infection is associated with increased IL-10 and IL-12 mRNA expression. The increased expression of IL-12 mRNA in the majority of patients with duodenal ulcer suggests that Th1 responses may predominate and play a role in the pathogenesis of duodenal ulceration.
authors.affiliation: Molecular Medicine Unit, St James's University Hospital, Leeds, UK.
authors.forename: N
authors.initials: N
authors.lastname: Hida
authors.forename: T
authors.initials: T
authors.lastname: Shimoyama
authors.forename: P
authors.initials: P
authors.lastname: Neville
authors.forename: M F
authors.initials: MF
authors.lastname: Dixon
authors.forename: A T
authors.initials: AT
authors.lastname: Axon
authors.forename: T
authors.initials: T
authors.lastname: Shimoyama
authors.forename: J E
authors.initials: JE
authors.lastname: Crabtree
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D000942:Antigens, Bacterial / Q000378:metabolism; D001426:Bacterial Proteins / Q000378:metabolism; D005260:Female; D005753:Gastric Mucosa / Q000276:immunology; D016481:Helicobacter Infections / Q000276:immunology* / Q000378:metabolism; D016480:Helicobacter pylori / Q000235:genetics* / Q000378:metabolism; D006801:Humans; D016753:Interleukin-10 / Q000096:biosynthesis* / Q000235:genetics; D018664:Interleukin-12 / Q000096:biosynthesis* / Q000235:genetics; D008297:Male; D008875:Middle Aged; D010437:Peptic Ulcer / Q000276:immunology / Q000378:metabolism / Q000382:microbiology*; D012333:RNA, Messenger / Q000096:biosynthesis; D020133:Reverse Transcriptase Polymerase Chain Reaction; D015854:Up-Regulation
chemical_list: D000942:Antigens, Bacterial; D001426:Bacterial Proteins; D012333:RNA, Messenger; C080866:cagA protein, Helicobacter pylori; D016753:Interleukin-10; D018664:Interleukin-12