House dust mite(HDM) antigen is one of the most common allergens associated with extrinsic asthma. In a model of allergic lung disease, Brown Norway rats sensitized to HDM with alum and Bordetella pertussis adjuvants produce high levels of IgE antibody and experience bronchoconstriction, increased airway hyperreactivity, and pulmonary inflammation after antigen challenge. To determine whether this allergic state could be transferred from sensitized animals to naive recipients via humoral or cellular factors, syngeneic recipient rats were injected i.p. with 4X10(superscript)7 cells(pre-cultured overnight with either HDM or BSA, respectively) from lymph nodes of sensitized or control rats. Other groups received a tail vein injection of serum from either HDM-sensitized or control rats. Three days post-transfer, animals were placed in a Fenn plethysmograph to assess bronchoconstriction after antigen challenge. The next day pulmonary hyperreactivity was measured during I.V.infusion of acetylcholine. Pulmonary inflammation was then assessed in bronchoalveolar lavage(BAL) fluid and histopathological sections. Antigen challenge in rats injected with sensitized cells caused increases in pulmonary inflammation and increases in airway hyperreactivity, but no changes in immediate bronchoconstriction compared to control recipients. Serum transferred immediate bronchoconstriction but had no effect on airway hyperreactivity or on pulmonary inflammation. These data demonstrate that immune-mediated lung inflammation and airway hyperreactivity are promoted by antigen-specific cells, while immediate allergic responses are caused by serum factors. Future studies will focus on the isolation and subsequent transfer of serum factors and cell phenotypes to determine which specific components contribute to the pathophysiology of allergic lung disease.