PASSIVE TRANSFER OF IMMEDIATE HYPERSENSITIVITY AND AIRWAY HYPERRESPONSIVENESS BY ALLERGEN-SPECIFIC IMMUNOGLOBULIN (IG)-E AND IGG1 IN MICE

In a proportion of atopic asthmatics, exposure to a relevant antigen i s followed by chronic inflammation in the airways leading to altered a irway responsiveness (AR), However, the mechanisms underlying the deve lopment of airway hyperresponsiveness still remain unclear. To elucida te the relationship between IgE-mediated reactions and airway hyperres ponsiveness, a murine model of passive sensitization and airway challe nge with ovalbumin (OVA) was developed using anti-OVA IgE and IgG anti bodies from murine B cell hybridomas. Passive sensitization by intrave nous injection of anti-OVA IgE resulted in immediate cutaneous hyperse nsitivity and, after airway challenge with OVA on two consecutive days , increased AR in BALB/c and SJL mice. Increased numbers of eosinophil s were observed in bronchoalveolar lavage fluid, in cells extracted fr om the lungs, and in the peribronchial areas of BALB/c mice passively sensitized with IgE and challenged through the airways compared with n onsensitized mice. Eosinophil peroxidase activity was also elevated in lung tissue from these mice, Passive sensitization with anti-OVA IgG1 but not IgG2a or IgG3 was similarly associated with development of sk in test reactivity and increased AR after airway challenge, accompanie d by an increase in eosinophils in bronchoalveolar lavage fluid. These data suggest that IgE/IgG1-mediated reactions together with local cha llenge with antigen can result in allergic inflammation resulting in a ltered airway function.