title: Levels of interleukin-18 are markedly increased in Helicobacter pylori-infected gastric mucosa among patients with specific IL18 genotypes.
abstract: BACKGROUND
  The cellular immune response in gastric mucosa infected with Helicobacter pylori is proposed to be predominantly of the T helper cell type 1 type.
  
  
  METHODS
  Interleukin (IL)-18, IL-12, and interferon (IFN)-gamma levels were measured in gastric mucosal biopsy specimens by reverse-transcription polymerase chain reaction (PCR) and by enzyme-linked immunosorbent assay; IL18 polymorphisms were determined by PCR.
  
  
  RESULTS
  Biopsy specimens from 128 patients (56 with nonulcer dyspepsia, 28 with gastric ulcers, 28 with duodenal ulcers, and 16 with gastric cancer) were examined; 96 patients had H. pylori infection. IL-18 levels were markedly up-regulated in mucosa infected with H. pylori (P < .001), whereas IL-12 and IFN-gamma levels were independent of H. pylori status. IL-18 levels correlated with IFN-gamma levels only in infected patients (R = 0.31 to R = 0.51). IL-18 levels were the determining factor for monocyte infiltration in H. pylori-infected mucosa (P < .001). H. pylori-infected patients displaying IL18 -607C/C and -137G/G had higher IL-18 levels than did those with other genotypes and were more likely to experience treatment failure.
  
  
  CONCLUSIONS
  H. pylori infection induces IL-18 in the gastric mucosa. H. pylori-infected patients with IL18 -607C/C and -137G/G have higher IL-18 levels, which causes severe gastric inflammation. IL18 genotype might be a marker for predicting the effects of eradication therapy.
authors.affiliation: Department of Gastroenterology and Hepatology, Nara City Hospital, Nara, Japan.
authors.forename: Kyoko
authors.initials: K
authors.lastname: Sakai
authors.forename: Masakazu
authors.initials: M
authors.lastname: Kita
authors.forename: Naoki
authors.initials: N
authors.lastname: Sawai
authors.forename: Satoshi
authors.initials: S
authors.lastname: Shiomi
authors.forename: Yoshio
authors.initials: Y
authors.lastname: Sumida
authors.forename: Kazuyuki
authors.initials: K
authors.lastname: Kanemasa
authors.forename: Shoji
authors.initials: S
authors.lastname: Mitsufuji
authors.forename: Jiro
authors.initials: J
authors.lastname: Imanishi
authors.forename: Yoshio
authors.initials: Y
authors.lastname: Yamaoka
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000900:Anti-Bacterial Agents / Q000627:therapeutic use; D004381:Duodenal Ulcer / Q000235:genetics / Q000382:microbiology; D004415:Dyspepsia / Q000235:genetics / Q000382:microbiology; D005260:Female; D005753:Gastric Mucosa / Q000276:immunology / Q000382:microbiology*; D005819:Genetic Markers; D020022:Genetic Predisposition to Disease; D005838:Genotype; D016481:Helicobacter Infections / Q000188:drug therapy / Q000378:metabolism*; D016480:Helicobacter pylori; D006801:Humans; D007371:Interferon-gamma / Q000378:metabolism; D018664:Interleukin-12 / Q000378:metabolism; D020382:Interleukin-18 / Q000235:genetics* / Q000378:metabolism*; D008297:Male; D008875:Middle Aged; D011110:Polymorphism, Genetic; D013274:Stomach Neoplasms / Q000235:genetics / Q000382:microbiology; D013276:Stomach Ulcer / Q000235:genetics / Q000382:microbiology
chemical_list: D000900:Anti-Bacterial Agents; D005819:Genetic Markers; D020382:Interleukin-18; D018664:Interleukin-12; D007371:Interferon-gamma