Asthma is an atopic disorder characterised by the activation and recruitmen
t of eosinophils to the lung resulting in chronic swelling and inflammation
of the airways. Allergic disorders such as atopic asthma and dermatitis ha
ve been increasingly prevalent in developed countries, and the inverse corr
elation between exposure to major diseases such as tuberculosis and atopy p
revalence has been reported. Intranasal administration of Mycobacterium bov
is-Bacillus Calmette-Guerin (BCG) has been demonstrated to suppress airway
eosinophilia in a model of atopic asthma. This immunomodulation is attribut
ed to the ability of interferon (IFN)-gamma produced by BCG-specific T(H)1
lymphocytes to inhibit the development of lung T(H)2 responses such as airw
ay eosinophilia. The mechanism of IFN gamma-induced inhibition is yet to be
defined, but could involve activation of macrophages, direct suppression o
f developing T(H)2 lymphocytes, or altered dendritic cell activation and an
tigen presentation. Mycobacteria such as BCG and certain mycobacterial frac
tions are strong inducers of a T(H)1 immune response. The effectiveness of
BCG in inhibiting atopic airway eosinophilia suggests its potential as a us
eful therapeutic agent in the treatment of atopic asthma.