BCG INFECTION SUPPRESSES ALLERGIC SENSITIZATION AND DEVELOPMENT OF INCREASED AIRWAY REACTIVITY IN AN ANIMAL-MODEL

Background: Epidemiologic studies suggest an inverse correlation betwe en infections and development of atopy. The purpose of this study was to test the hypothesis whether a preexisting T-H1-type immune response elicited by BCG immunization could suppress allergic sensitization an d airway hyperreactivity in an animal model. Methods: BALB/c mice were immunized with BCG and/or sensitized to ovalbumin. Results: BCG immun ization alone resulted in cutaneous type-IV hypersensitivity reactions to tuberculin and granulomatous lesions in the liver. Splenic mononuc lear cells (MNCs) produced increased levels of IFN-gamma after activat ion by Concanavalin A (ConA). Ovalbumin sensitization alone resulted i n increased production of IL-4 after activation by ConA. Ovalbumin-sen sitized animals also demonstrated markedly elevated anti-ovalbumin IgE /IgG1 serum antibody titers and increased airway reactivity after alle rgen challenges by means of the airways. BCG immunization 14 days befo re the start of ovalbumin sensitization markedly hindered the developm ent 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 oval bumin restimulation, (3) partial prevention of ovalbumin-specific IgE/ IgG1 serum antibody titers but elevated (nonallergic) anti-ovalbumin I gG2a 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. Conclusion: In this model BCG immunization established a T-H1-type immune respons e that hinders allergic sensitization and the development of increased airway reactivity.