title: BCG infection suppresses allergic sensitization and development of increased airway reactivity in an animal model.
abstract: BACKGROUND
  Epidemiologic studies suggest an inverse correlation between infections and development of atopy. The purpose of this study was to test the hypothesis whether a preexisting Th1-type immune response elicited by BCG immunization could suppress allergic sensitization and airway hyperreactivity in an animal model.
  
  
  METHODS
  BALB/c mice were immunized with BCG and/or sensitized to ovalbumin.
  
  
  RESULTS
  BCG immunization alone resulted in cutaneous type-IV hypersensitivity reactions to tuberculin and granulomatous lesions in the liver. Splenic mononuclear cells (MNCs) produced increased levels of IFN-gamma after activation by Concanavalin A (ConA). Ovalbumin sensitization alone resulted in increased production of IL-4 after activation by ConA. Ovalbumin-sensitized animals also demonstrated markedly elevated anti-ovalbumin IgE/IgG1 serum antibody titers and increased airway reactivity after allergen challenges by means of the airways. BCG immunization 14 days before the start of ovalbumin sensitization markedly hindered the development of allergic responses as indicated by (1) increased IFN-gamma and normalized IL-4 and IL-10 production by splenic MNCs after activation with ConA, (2) a reduced proliferation rate of splenic MNCs after ovalbumin restimulation, (3) partial prevention of ovalbumin-specific IgE/IgG1 serum antibody titers but elevated (nonallergic) anti-ovalbumin IgG2a serum antibody titers, (4) prevention of airway responsiveness, (5) reduced eosinophilic influx into the airway lumen, and (6) reduced levels of IL-4 and IL-5 in broncho alveolar lavage fluids.
  
  
  CONCLUSIONS
  In this model BCG immunization established a Th1-type immune response that hinders allergic sensitization and the development of increased airway reactivity.
authors.affiliation: Departments of Laboratory Medicine and Pathobiochemistry and Pediatric Pulmonology and Immunology, Charité, Campus Virchow-Clinic, Berlin, Germany.
authors.forename: U
authors.initials: U
authors.lastname: Herz
authors.forename: K
authors.initials: K
authors.lastname: Gerhold
authors.forename: C
authors.initials: C
authors.lastname: Grüber
authors.forename: A
authors.initials: A
authors.lastname: Braun
authors.forename: U
authors.initials: U
authors.lastname: Wahn
authors.forename: H
authors.initials: H
authors.lastname: Renz
authors.forename: K
authors.initials: K
authors.lastname: Paul
mesh_terms: D000818:Animals; D001249:Asthma / Q000276:immunology* / Q000503:physiopathology / Q000517:prevention & control; D001500:BCG Vaccine / Q000276:immunology*; D016535:Bronchial Hyperreactivity / Q000517:prevention & control; D001992:Bronchoalveolar Lavage Fluid / Q000737:chemistry; D004195:Disease Models, Animal; D005260:Female; D006968:Hypersensitivity, Delayed / Q000276:immunology; D007114:Immunization; D015847:Interleukin-4 / Q000378:metabolism; D015848:Interleukin-5 / Q000378:metabolism; D051379:Mice; D008807:Mice, Inbred BALB C; D010047:Ovalbumin / Q000276:immunology; D018417:Th1 Cells / Q000502:physiology
chemical_list: D001500:BCG Vaccine; D015848:Interleukin-5; D015847:Interleukin-4; D010047:Ovalbumin