Abstract
A model of secondary immune response in the middle ear (ME) was developed in the guinea pig. Animals were immunized intradermally with keyhole limpet hemocyanin (KLH) and challenged with KLH in the ME 8 weeks later. The ME displayed effusion, mucosal hyperplasia, mucosal edema, and leukocytic infiltration. These responses were maximal at 3 days postchallenge, and persisted for 2 to 3 weeks. High levels of antibody were observed in the ME effusions, and serum titers increased significantly. Immunohistochemical localization of antibody indicated that substantial free IgG was present in the submucosa, with much less in the mucosal epithelium. IgA plasma cells were observed in the submucosa at 1 week postchallenge, but no IgM was detected. In contrast to the response observed in sensitized animals, antigen presented to the ME of unimmunized control animals resulted in no effusion, minimal mucosal inflammation, and little or no antibody in either the ME or serum. However, substantial neutrophilic infiltration of the ME cavity was observed. The effusion and inflammation produced by secondary ME immune responses were not affected by tympanostomy tubes. Eustachian tube function as measured by a forced response test was not affected by ME immune response. This suggests that the immunologically induced effusion was not the result of eustachian tube obstruction. We postulate that increased vascular permeability in the ME mucosa, induced by chemical mediators, resulted in the transudation of serum.
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