This project involves use of a new animal model to study the basic pathogenetic mechanisms that may be involved in immunologic lung disease caused by reactive chemicals of low molecular weight (<1000 daltons). Current evidence suggests that such chemicals can combine with self-proteins to form hapten-protein conjugates that induce immunologic responses that cause lung disease. This project will extend and study the demonstration by us that serum containing human IgE to reactive chemical protein conjugates can passively transfer an asthmatic response from humans to monkeys. Thus, this would demonstrate the role in humans of such IgE antibodies in the pathogenesis of asthma caused by such reactive chemicals. Other passive transfer experiments will be used to confirm in vitro experiments that suggest an entirely new hypersensitivity mechanism that may result from human exposure to chemicals capable of acting as haptens. In this mechanism, non-IgE antihapten antibodies react with hapten-modified IgE and hapten-modified cell surfaces (e.g. basophils, mast cells) to cause bronchospasm.
