FAILURE OF AGED RATS TO ACCUMULATE EOSINOPHILS IN ALLERGIC INFLAMMATION OF THE AIRWAY

To investigate the effect of aging on the allergic airway response, we examined the bronchoconstrictive responses and cellular inflammatory changes in a rat model of bronchial asthma by evaluating young and old animals. Two different age groups of Brown-Norway rats, actively sens itized by injection of ovalbumin into the foot pads, were used: 7 to 8 weeks old (young group) and 100 to 120 weeks old (aged group). Both t he aged and young rats produced an ovalbumin-specific IgE antibody and exhibited an immediate asthmatic response after exposure to ovalbumin , but the degree of specific IgE antibody was significantly higher in young rats. The young group showed a marked increase in the number of eosinophils and neutrophils in bronchoalveolar lavage fluid 2 days aft er exposure to ovalbumin, whereas no eosinophilia was seen in the aged group. To evaluate the mechanism of the decreased accumulation of eos inophils in aged rats, cells from popliteal lymph nodes from ovalbumin -sensitized rats were incubated with ovalbumin for 48 hours. Although eosinophil chemotactic activity, determined by a modified Boyden chamb er method, was present in the supernatant of cultured lymph node cells from young rats, it was absent from those of aged rats. In vivo admin istration of anti-IL-5 monoclonal antibody revealed that one of the fa ctors of eosinophil chemotactic activity was IL-5. Lymph node cells fr om aged rats tended to produce greater amounts of interferon-gamma tha n did those from young animals. Findings indicate that aged rats have a defect in eosinophil accumulation in sites exposed to antigen, proba bly because of an age-dependent alteration in T cells.