Suppression of immediate and late responses to antigen by a non-anaphylactogenic anti-IgE antibody in a murine model of asthma

Eosinophils are recruited to the airways during allergic reactions, but ani mal models have shown that their mere presence is not sufficient for the de velopment of bronchopulmonary hyperreactivity. Other factors, such as immun oglobulin (Ig)E, seem to be required. Using mice selected for the production of large amounts of IgE, the effects of antibody neutralization of IgE on antigen-induced lung recruitment of e osinophils and induction of bronchopulmonary hyperreactivity and of other i ndicators of inflammation were studied. A monoclonal non-anaphylactogenic rat anti-mouse IgE (mAb1-5), given within 24 h of the challenge with antigen, reduced tissue eosinophilia, the recru itment of IgE-bearing cells identified as basophils, mucous cell metaplasia , anaphylactic bronchoconstriction and bronchopulmonary hyperreactivity. mA b1-5 inhibited interleukin (IL)-4 titres in the bronchoalveolar lavage flui d, but not those of IL-5. Inhibition by mAb1-5 may result from competitive displacement of immunoglob ulin E from its different receptors, thus preventing cell stimulation. More over, the inhibition of the massive recruitment of immunoglobulin E-bearing basophils into the lungs within hours after challenge and of interleukin-4 production by mAb1-5 may be important factors leading to the reduction of pulmonary eosinophilia and bronchopulmonary hyperreactivity. Thus, immunogl obulin (Ig)E and allergic IgE-bearing cells seem to play an essential role in the initial development of the late allergic airway responses.