title: Helicobacter pylori cag pathogenicity island is associated with enhanced interleukin-8 expression in human gastric mucosa.
abstract: BACKGROUND
  In vitro studies showed that Helicobacter pylori strains carrying the cag pathogenicity island are able to induce epithelial secretion of Interleukin-8.
  
  
  OBJECTIVE
  To evaluate the assessment of cag pathogenicity island and the expression of Interleukin-8 in the gastric mucosa of Helicobacter pylori-infected patients and correlate these data with the activity of gastritis and Helicobacter pylori density.
  
  
  METHODS
  cag status was determined by polymerase chain reaction directly on gastric biopsies from 13 Helicobacter pylori+ patients with non-ulcer dyspepsia and 13 Helicobacter pylori+ with duodenal ulcer. Interleukin-8 gene transcription and protein expression were analysed by in situ hybridization and immunofluorescence, respectively. Gastritis activity and Helicobacter pylori density were also investigated.
  
  
  RESULTS
  cag was present in 20/26 of Helicobacter pylori+ patients: in 7/13 non-ulcer dyspepsia (53.8%] and in 13/13 duodenal ulcer patients (100%), (p<0.05). Interleukin-8 mRNA and protein expression in epithelial and inflammatory cells was higher in cag+ than in cag- patients (p<0.005). Gastritis activity significantly correlated with cag (p<0.05) and Interleukin-8 expression (p<0.005]. Helicobacter pylori density was enhanced in cag+ [p<0.005] and correlated with Interleukin-8 expression (p<0.0051.
  
  
  CONCLUSIONS
  The present study demonstrates that in Helicobacter pylori-infected human gastric mucosa, cag+ infection is associated with enhanced Interleukin-8 expression, higher levels of active gastritis and bacterial density, and presence of duodenal ulcer.
authors.affiliation: Department of Clinical Pathophysiology, University of Florence, Italy.
authors.forename: B
authors.initials: B
authors.lastname: Orsini
authors.forename: G
authors.initials: G
authors.lastname: Ciancio
authors.forename: S
authors.initials: S
authors.lastname: Censini
authors.forename: E
authors.initials: E
authors.lastname: Surrenti
authors.forename: G
authors.initials: G
authors.lastname: Pellegrini
authors.forename: S
authors.initials: S
authors.lastname: Milani
authors.forename: H
authors.initials: H
authors.lastname: Herbst
authors.forename: A
authors.initials: A
authors.lastname: Amorosi
authors.forename: C
authors.initials: C
authors.lastname: Surrenti
mesh_terms: D000942:Antigens, Bacterial; D001426:Bacterial Proteins / Q000096:biosynthesis / Q000235:genetics*; D004381:Duodenal Ulcer / Q000382:microbiology*; D005753:Gastric Mucosa / Q000382:microbiology; D005756:Gastritis / Q000382:microbiology; D005786:Gene Expression Regulation; D016481:Helicobacter Infections / Q000382:microbiology*; D016480:Helicobacter pylori / Q000235:genetics* / Q000472:pathogenicity*; D006801:Humans; D017403:In Situ Hybridization; D016209:Interleukin-8 / Q000096:biosynthesis*; D016133:Polymerase Chain Reaction
chemical_list: D000942:Antigens, Bacterial; D001426:Bacterial Proteins; D016209:Interleukin-8; C080866:cagA protein, Helicobacter pylori