INFECTION OF MICE WITH MYCOBACTERIUM-BOVIS-BACILLUS CALMETTE-GUERIN (BCG) SUPPRESSES ALLERGEN-INDUCED AIRWAY EOSINOPHILIA

It has been proposed that the increase in prevalence and severity of a topic disorders inversely corn-elates with exposure to infectious dise ases such as tuberculosis. We have investigated this issue by combinin g an intranasal Mycobacterium bovis-Bacillus Calmette-Guerin (BCG) inf ection with a murine model of allergen, (ovalbumin [OVA]) induced airw ay eosillophilia. BCG infection either 4 or 12 wk before allergen airw ay challenge resulted in a 90-95 and 60-70% reduction in eosinophilia within the lungs, respectively, compared to uninfected controls. The i nhibition of airway eosinophilia correlated with a reduced level of IL -5 production by T cells from the lymph node draining the site of OVA challenge. Interestingly, BCG infection of the lung had no effect on I gG1 and IgE OVA-specific serum immunoglobulin or blood eosinophil leve ls. Furthermore, BCG-induced inhibition of airway eosinophilia was str ongly reduced in interferon (IFN)-gamma receptor-deficient mice and co uld be partially reversed by intranasal IL-5 application. lntranasal B CG infections could also reduce the degree of lung eosinophilia and IL -5 produced by T cells after Nippostrongylus brasiliensis infection. T aken together, our data suggest that IFN-gamma produced during the T h elper cell (Th) 1 immune response against BCG suppresses the developme nt of local inflammatory Th2 responses in the lung. Most importantly, this inhibition did not extend to the systemic immunoglobulin response against OVA. Our data support the view that mycobacterial infections have the potential to suppress the development of atopic disorders in humans.