Yi-Hao Lin; Guiming Liu; Vince Tuohy; Firouz Daneshgari; Cleveland, Ohio

Objectives: Interstitial cystitis (IC) is a chronic bladder disorder, manifested by frequency, urgency of urination, with plausible autoimmune pathogenesis. We aimed to examine the bladder function of our recently developed experimental autoimmune cystitis (EAC) model in female SWXJ mice.

Materials and Methods: Twenty SWXJ female mice were divided into two groups; EAC group injected with Completed Freund’s Adjuvant (CFA) containing bladder homogenate carried by M. Tuberculosis and control group injected with CFA alone. Six months after injections, bladder function of animals was studied with 24-hour micturition habits using metabolic cages. Subsequently, the animals underwent conscious cystometrogram (CMG) two days after implantation of suprapubic bladder tube. After completion of CMG, the animals were euthanized and their bladders were harvested for histologic examination. The data were analyzed using student t-test, with P<0.05 indicating a significant difference.

Results: 24-hour micturition habits showed EAC group to have a higher frequency of micturition than control group (p<0.05). Conscious CMG showed significantly shorter intercontraction interval in the EAC group compared to controls (163.84 ± 22.24 vs 487.30 ± 84.90 sec, respectively) confirming the higher frequency of micturition cycles in the EAC group. Voided volume per micturition was significantly lower in EAC group compared to controls (0.062± 0.005, 0.078± 0.005. respectively). There were no significant differences in peak voiding pressure between the experimental and control group (p=0.448). Histology examination showed the thickened lamina propria and significant infiltration of mast cells, lymphocytes and giant cells in the bladder of EAC animals.

Conclusions: Our experimental autoimmune cystitis model has similar features to those observed in human IC, and may provide a model for the study of the pathogenesis and treatment of interstitial cystitis. Further studies are warranted to characterize and investigate the autoimmune mechanisms of EAC model.

Source of Funding: Supported by grants NIH-NIDDK-DK02631; U01-DK61018; Young-Investigator award of the National Kidney Foundation; Grant-in aid by the Diabetic Association of the Greater Cleveland; and Juvenile Diabetes Research Foundation Fellowship (to G. Liu).

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