title: Interleukin-17 is a critical mediator of vaccine-induced reduction of Helicobacter infection in the mouse model.
abstract: OBJECTIVE
  Despite the proven ability of immunization to reduce Helicobacter infection in mouse models, the precise mechanism of protection has remained elusive. This study explores the possibility that interleukin (IL)-17 plays a role in the reduction of Helicobacter infection following vaccination of wild-type animals or in spontaneous reduction of bacterial infection in IL-10-deficient mice.
  
  
  METHODS
  In mice, reducing Helicobacter infection, the levels and source of IL-17 were determined and the role of IL-17 in reduction of Helicobacter infection was probed by neutralizing antibodies.
  
  
  RESULTS
  Gastric IL-17 levels were strongly increased in mice mucosally immunized with urease plus cholera toxin and challenged with Helicobacter felis as compared with controls (654 +/- 455 and 34 +/- 84 relative units for IL-17 messenger RNA expression [P < .01] and 6.9 +/- 8.4 and 0.02 +/- 0.04 pg for IL-17 protein concentration [P < .01], respectively). Flow cytometry analysis showed that a peak of CD4(+)IL-17(+) T cells infiltrating the gastric mucosa occurred in immunized mice in contrast to control mice (4.7% +/- 0.3% and 1.4% +/- 0.3% [P < .01], respectively). Gastric mucosa-infiltrating CD4(+)IL-17(+) T cells were also observed in IL-10-deficient mice that spontaneously reduced H felis infection (4.3% +/- 2.3% and 2% +/- 0.6% [P < .01], for infected and noninfected IL-10-deficient mice, respectively). In wild-type immunized mice, intraperitoneal injection of anti-IL-17 antibodies significantly inhibited inflammation and the reduction of Helicobacter infection in comparison with control antibodies (1 of 12 mice vs 9 of 12 mice reduced Helicobacter infection [P < .01], respectively).
  
  
  CONCLUSIONS
  IL-17 plays a critical role in the immunization-induced reduction of Helicobacter infection from the gastric mucosa.
authors.affiliation: Division of Gastroenterology and Hepatology, Centre Hospitalier Universitaire Vaudois and University of Lausanne, Lausanne, Switzerland. dominique.velin@chuv.ch
authors.forename: Dominique
authors.initials: D
authors.lastname: Velin
authors.forename: Laurent
authors.initials: L
authors.lastname: Favre
authors.forename: Eric
authors.initials: E
authors.lastname: Bernasconi
authors.forename: Daniel
authors.initials: D
authors.lastname: Bachmann
authors.forename: Catherine
authors.initials: C
authors.lastname: Pythoud
authors.forename: Essia
authors.initials: E
authors.lastname: Saiji
authors.forename: Hanifa
authors.initials: H
authors.lastname: Bouzourene
authors.forename: Pierre
authors.initials: P
authors.lastname: Michetti
mesh_terms: D000818:Animals; D001428:Bacterial Vaccines / Q000494:pharmacology*; D016207:Cytokines / Q000378:metabolism; D004195:Disease Models, Animal; D005260:Female; D005434:Flow Cytometry; D005753:Gastric Mucosa / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D016481:Helicobacter Infections / Q000276:immunology* / Q000378:metabolism / Q000517:prevention & control; D016480:Helicobacter pylori / Q000276:immunology*; D007150:Immunohistochemistry; D007156:Immunologic Memory / Q000502:physiology*; D016753:Interleukin-10 / Q000172:deficiency / Q000276:immunology; D020381:Interleukin-17 / Q000276:immunology / Q000378:metabolism*; D051379:Mice; D008810:Mice, Inbred C57BL; D009195:Peroxidase / Q000378:metabolism; D016133:Polymerase Chain Reaction; D011336:Probability; D011897:Random Allocation; D012680:Sensitivity and Specificity; D018709:Statistics, Nonparametric; D018417:Th1 Cells / Q000276:immunology
chemical_list: D001428:Bacterial Vaccines; D016207:Cytokines; D020381:Interleukin-17; D016753:Interleukin-10; D009195:Peroxidase