title: Proinflammatory cytokine expression in gastric tissue from children with Helicobacter pylori-associated gastritis.
abstract: BACKGROUND
  Helicobacter pyloriinfection of the gastric mucosa in humans is usually acquired early in life. The chronic inflammation that ensues involves the increased production of inflammatory cytokines. Published data on production of these mediators by gastric mucosa of H. pylori-infected children are few.
  
  
  METHODS
  Seventy-nine children, aged 5 to 18 years, referred for upper gastrointestinal endoscopy to four separate hospitals in Chile, were studied. The concentrations of interleukin (IL)-1beta, IL-6, IL-8, and tumor necrosis factor alpha were measured in homogenates of gastric mucosal biopsy specimens. Cytokine expression was confirmed by reverse transcription polymerase chain reaction. These data were correlated with the patients' clinical, histologic and sociodemographic status.
  
  
  RESULTS
  Patient rate of colonization by H. pylori was inversely correlated with socioeconomic status (P < 0.005) and positively correlated with age (P < 0.0025). In gastric mucosa, concentrations of IL-1beta, IL-8, and tumor necrosis factor alpha were all significantly higher in H. pylori-positive patients than in H. pylori-negative patients and in patients who had histologic gastritis than in those with normal gastric mucosa. In patients with peptic ulcer disease, only IL-1beta and IL-8 concentrations were significantly elevated when compared with those of patients without ulcers. Interleukin-6 concentrations were comparable among the different groups analyzed.
  
  
  CONCLUSIONS
  This study suggests that increased gastric mucosal production of the proinflammatory cytokines IL-1beta and IL-8 is probably involved in H. pylori-associated gastric damage in children and may be crucial in determining the different clinical outcomes.
authors.affiliation: Departamentos de Pediatría y Anatomía Patológica, Pontificia Universidad Católica de Chile, Santiago, Chile. eguirald@puc.cl
authors.forename: E
authors.initials: E
authors.lastname: Guiraldes
authors.forename: I
authors.initials: I
authors.lastname: Duarte
authors.forename: A
authors.initials: A
authors.lastname: Peña
authors.forename: A
authors.initials: A
authors.lastname: Godoy
authors.forename: M N
authors.initials: MN
authors.lastname: Espinosa
authors.forename: R
authors.initials: R
authors.lastname: Bravo
authors.forename: F
authors.initials: F
authors.lastname: Larraín
authors.forename: M
authors.initials: M
authors.lastname: Schultz
authors.forename: P
authors.initials: P
authors.lastname: Harris
mesh_terms: D000293:Adolescent; D000367:Age Factors; D001706:Biopsy; D002648:Child; D002675:Child, Preschool; D004724:Endoscopy; D005260:Female; D005753:Gastric Mucosa / Q000276:immunology / Q000382:microbiology* / Q000473:pathology; D005756:Gastritis / Q000276:immunology* / Q000382:microbiology* / Q000473:pathology; D016481:Helicobacter Infections / Q000276:immunology* / Q000382:microbiology* / Q000473:pathology; D016480:Helicobacter pylori / Q000276:immunology*; D006801:Humans; D007375:Interleukin-1 / Q000096:biosynthesis / Q000378:metabolism; D015850:Interleukin-6 / Q000096:biosynthesis / Q000378:metabolism; D016209:Interleukin-8 / Q000096:biosynthesis / Q000378:metabolism; D008297:Male; D010437:Peptic Ulcer / Q000276:immunology / Q000382:microbiology / Q000473:pathology; D020133:Reverse Transcriptase Polymerase Chain Reaction; D012923:Social Class; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis / Q000378:metabolism
chemical_list: D007375:Interleukin-1; D015850:Interleukin-6; D016209:Interleukin-8; D014409:Tumor Necrosis Factor-alpha