Mast cell-deficient mice develop a reaginic antibody immune response

In using a mast cell-deficient mouse model to investigate the role of mast cells and immediate-type hypersensitivity in antigen-induced bladder inflammation, we initially sought to demonstrate that mast cell-deficient mice can mount a reaginic antibody response. Mast cell-deficient (w/wv) mice and congenic controls (+/+) were actively sensitized by repeated injections of dinitrophenol-ovalbumin (DNP-OVA). Serum IgE was measured by ELISA before and after DNP-OVA. After 4 weeks, the urinary bladders were removed and suspended in a tissue bath. Smooth muscle contraction and histamine release were monitored upon challenge of bladder tissue by superfusion with DNP-HSA. In similar experiments, serum from sensitized mice was used for passive sensitization of bladder tissue from naive mice. Pre-sensitization serum IgE was similar in w/wv and +/+ mice (0.4 vs. 0.3 μg/ml); IgE levels increased significantly in both groups after active sensitization (to 2.9 vs. 2.0 μg/ml). Bladders from actively-sensitized w/wv mice failed to respond to antigen challenge, whereas those from actively-sensitized +/+ mice responded with contraction and histamine release. Bladders isolated from naive +/+ mice, when passively sensitized with serum from sensitized w/wv mice, also contracted upon antigen stimulation. These studies demonstrate that w/wv mast cell deficient mice produce functional reaginic antibodies; the experimental approach described can provide quantitative data and will aid in defining the role of mast cells in bladder inflammatory reactions.