title: Immunosuppression of TH2 responses in Trichinella spiralis infection by Helicobacter pylori neutrophil-activating protein.
abstract: BACKGROUND
  The Helicobacter pylori neutrophil-activating protein (HP-NAP) is able to induce IL-12 expression by cells of innate immunity and to shift to T(H)1 human allergen-specific T(H)2 cells in vitro.
  
  
  OBJECTIVE
  We performed an in vivo investigation of the ability of HP-NAP to downmodulate the T(H)2 response induced in mice by Trichinella spiralis infection.
  
  
  METHODS
  Groups of T spiralis-infected BALB/c mice received intraperitoneal PBS/rat IgG2b (control animals) or 10 microg of HP-NAP with or without anti-Toll-like receptor 2 antibody on days 10 and 28 after infection. Blood eosinophils, total and T spiralis-specific IgE levels, and cytokine levels were measured in the plasma up to day 42, when splenocytes were cultured for cytokine production.
  
  
  RESULTS
  Although control animals showed significant eosinophilia and increase of total and T spiralis-specific IgE, IL-4, and IL-5 levels from days 10 to 14, HP-NAP-treated animals showed less eosinophilia and total and excretory/secretory antigens of T spiralis-specific IgE in the blood. HP-NAP-treated animals also had higher IL-12 and IFN-gamma plasma levels and lower IL-4 and IL-5 levels. The addition of anti-Toll-like receptor 2 antibody abrogated the anti-T(H)2/pro-T(H)1 activity of HP-NAP.
  
  
  CONCLUSIONS
  This study provides evidence that HP-NAP enhances endogenous IL-12 and IFN-gamma response and exerts a powerful anti-T(H)2 activity in vivo, targeting both IL-5-induced eosinophilia and IL-4-mediated hyper-IgE responses induced by parasitic infection.
authors.affiliation: Department of Internal Medicine, University of Florence, Florence, Italy. gdelprete@unifi.it
authors.forename: Gianfranco
authors.initials: G
authors.lastname: Del Prete
authors.forename: Lorena
authors.initials: L
authors.lastname: Chiumiento
authors.forename: Amedeo
authors.initials: A
authors.lastname: Amedei
authors.forename: Maria
authors.initials: M
authors.lastname: Piazza
authors.forename: Mario M
authors.initials: MM
authors.lastname: D'Elios
authors.forename: Gaia
authors.initials: G
authors.lastname: Codolo
authors.forename: Marina
authors.initials: M
authors.lastname: de Bernard
authors.forename: Massimo
authors.initials: M
authors.lastname: Masetti
authors.forename: Fabrizio
authors.initials: F
authors.lastname: Bruschi
mesh_terms: D000818:Animals; D000942:Antigens, Bacterial / Q000276:immunology; D001426:Bacterial Proteins / Q000276:immunology*; D004195:Disease Models, Animal; D015536:Down-Regulation; D004802:Eosinophilia / Q000276:immunology; D005260:Female; D007073:Immunoglobulin E / Q000276:immunology; D007371:Interferon-gamma / Q000276:immunology; D018664:Interleukin-12 / Q000276:immunology; D015847:Interleukin-4 / Q000276:immunology; D015848:Interleukin-5 / Q000276:immunology; D051379:Mice; D008807:Mice, Inbred BALB C; D018417:Th1 Cells / Q000276:immunology; D018418:Th2 Cells / Q000276:immunology*; D017160:Trichinella spiralis; D014235:Trichinellosis / Q000276:immunology*
chemical_list: D000942:Antigens, Bacterial; D001426:Bacterial Proteins; D015848:Interleukin-5; C092412:neutrophil-activating protein A, Helicobacter pylori; D018664:Interleukin-12; D015847:Interleukin-4; D007073:Immunoglobulin E; D007371:Interferon-gamma