OBJECTIVE To examine bladder function in a newly developed experimental autoimmune cystitis (EAC) model in female SWXJ strain mice, as a potential animal model for interstitial cystitis (IC). MATERIALS AND METHODS In all, 20 SWXJ female mice were divided into two groups: an EAC group immunized with mouse bladder homogenate in complete Freund’s adjuvant (CFA) and a control group immunized with CFA alone. At 4 months after injection, the bladder function of some mice (six) was studied with 24‐h micturition habits using metabolic cages and conscious cystometrography (CMG). The bladder and lung were harvested for histological examination and to assess interferon‐γ (IFN‐γ) mRNA expression. RESULTS Histology examination showed obviously thickened lamina propria, infiltration of lymphocytes, giant cells, and increased mast cells in the detrusor muscle of the EAC mice. The lungs of EAC mice showed normal histology. The IFN‐γ mRNA expression increased significantly in the bladder, but not in the lung of the EAC mice. The 24‐h micturition habits measurements showed increased frequency of urination in the EAC mice compared with the controls. Similarly, CMG showed decreased intercontraction intervals and voided volumes per micturition in the EAC mice compared with the controls. However, there were no significant differences in peak voiding pressure or total voiding volume between the EAC and control mice. CONCLUSIONS Our murine EAC model has comparable functional and histological alterations to those seen in human IC, and may provide a useful model for the study of the pathogenesis and treatment of IC.

The effects of obesity and type 2 diabetes (DMII) on the lower urinary tract (LUT) were characterized by evaluating voiding function and anatomy in female Zucker diabetic fatty (ZDF) rats. Age-matched female virgin rats were separated into three experimental groups: Zucker lean rats (control; normal diet, n = 22), ZDF rats (obese+nondiabetic; low-fat diet, n = 22), and ZDF rats (obese+diabetic; high-fat diet, n = 20). Rats were placed on their specified diet for 10 wk before urodynamic LUT evaluation. A suprapubic catheter was implanted 2 days before urodynamic studies. Voiding function was evaluated by cystometric and leak point pressure (LPP) testing. The bladder, urethra, and vagina were immediately excised for qualitative histological evaluation. Compared with control rats, obese+nondiabetic and obese+diabetic rats had significantly decreased contraction pressure ( P = 0.003) and increased cystometric filling volume ( P < 0.001). Both obese groups exhibited significantly higher voided volumes ( P = 0.003), less frequent urinary events ( P < 0.001), and increased residual volumes ( P = 0.039). LPP studies showed a nonsignificant decrease in LPP ( P = 0.075) and baseline pressure ( P = 0.168) in both obese groups compared with control. Histology of the external urethral sphincter in obese rats showed increased fibrosis, leading to disruption of the skeletal muscle structure compared with control. Additionally, the bladder wall of the obese+nondiabetic and obese+diabetic rats demonstrated edema and vasculopathy. Voiding dysfunction was evident in both obese groups but with no significant differences due to DMII, suggesting that voiding dysfunction in DMII may be attributable at least in part to chronic obesity.

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