title: IL-17 is involved in Helicobacter pylori-induced gastric inflammatory responses in a mouse model.
abstract: BACKGROUND
  Helicobacter pylori (H. pylori) is the major cause of chronic active gastritis and peptic ulcer disease. Recent studies have shown that H. pylori produces various cytokines that are related to neutrophil or mononuclear cell accumulation. Interleukin-17 (IL-17) is the founding member of an emerging family of inflammatory cytokines whose biological activities remain incompletely defined. In this study, the contributions of IL-17 to the induction of gastric inflammation and to the protection from H. pylori infection were investigated using IL-17 gene-knockout (IL-17(-/-)) mice.
  
  
  METHODS
  IL-17(-/-)and wild-type C57BL/6 mice were challenged with H. pylori CPY2052 (2 x 10(8) CFU/mL) and the histological and microbiological evaluation were carried out at specified times. IL-17 and myeloperoxidase (MPO) protein levels in tissues were assayed in duplicate using ELISA kits.
  
  
  RESULTS
  In wild-type mice, IL-17 was undetected at baseline; however, the protein expression of IL-17 was induced after infection with H. pylori. A severe infiltration of neutrophils appeared in the submucosa and the lamina propria in wild-type mice. In contrast, the degree of neutrophil infiltration in IL-17(-/-) mice was significantly lower than that in wild-type mice. Although wild-type mice infected with H. pylori showed drastically higher MPO activity compared with uninfected wild-type mice, any significant increase in the enzyme activity was not revealed in infected IL-17(-/-) mice. The number of H. pylori colonized in the stomach of IL-17(-/-) mice was significantly lower than that of wild-type mice from 1 to 6 months after infection.
  
  
  CONCLUSIONS
  These results suggest that IL-17 may play an important role in the inflammatory response to the H. pylori infection and ultimately influence the outcome of the H. pylori-associated disease.
authors.affiliation: Department of Microbiology, Kyoto Prefectural University of Medicine, Kyoto, Japan.
authors.forename: Satoshi
authors.initials: S
authors.lastname: Shiomi
authors.forename: Akihiro
authors.initials: A
authors.lastname: Toriie
authors.forename: Shigeyoshi
authors.initials: S
authors.lastname: Imamura
authors.forename: Hideyuki
authors.initials: H
authors.lastname: Konishi
authors.forename: Shoji
authors.initials: S
authors.lastname: Mitsufuji
authors.forename: Yoichiro
authors.initials: Y
authors.lastname: Iwakura
authors.forename: Yoshio
authors.initials: Y
authors.lastname: Yamaoka
authors.forename: Hiroyoshi
authors.initials: H
authors.lastname: Ota
authors.forename: Toshiro
authors.initials: T
authors.lastname: Yamamoto
authors.forename: Jiro
authors.initials: J
authors.lastname: Imanishi
authors.forename: Masakazu
authors.initials: M
authors.lastname: Kita
mesh_terms: D000818:Animals; D015169:Colony Count, Microbial; D005753:Gastric Mucosa / Q000737:chemistry / Q000276:immunology* / Q000382:microbiology / Q000473:pathology*; D016481:Helicobacter Infections / Q000276:immunology* / Q000473:pathology*; D016480:Helicobacter pylori / Q000276:immunology*; D006801:Humans; D020381:Interleukin-17 / Q000172:deficiency / Q000276:immunology*; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D009504:Neutrophils / Q000276:immunology; D009195:Peroxidase / Q000032:analysis
chemical_list: D020381:Interleukin-17; D009195:Peroxidase