Interstitial Cystitis (IC) is a painful bladder condition which may have an autoimmune etiology. As detailed previously, an autoimmune animal model for the disease has been developed called Experimental Autoimmune Cystitis (EAC) which is induced by injecting female Lewis rats with bladder homogenates in Freund's adjuvant. The animal model has been shown to exhibit elevated urinary frequency, the hallmark of IC. This symptom was transferable to naive, syngeneic animals via spenocyte transfer. However, inflammatory infiltrates were not common in either primary or secondary EAC. Studies presented here investigate the possibility that a soluble substance, for example an autoantibody, is responsible for the symptoms of the disease. Western Blots were used to identify an autoantibody in the serum of EAC animals specific to the disease. The antibody was found present in sera from EAC animals but not in sera from sham animals and bladder antigen injected animals (BAIA) which were injected with bladder antigens but did not respond with elevated urianry frequency. The target antigen of this autoantibody is a bladder protein with a molecular weight of 12kD. Initial purification of this protein using gel electrophoresis and electroelution is reported here. Further purification and identification of this target antigen may explain the pathogenesis which leads to increased urinary frequency in these animals and potentially in IC patients as well.
Worcester Polytechnic Institute
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Biology and Biotechnology