Original Paper

Urological Research

, Volume 24, Issue 6, pp 367-373

Experimental autoimmune cystitis in the Lewis rat: a potential animal model for interstitial cystitis

  • J. Luber-NarodAffiliated withDivision of Urologic and Transplantation Surgery, Department of Surgery, University of Massachusetts Medical School
  • , T. Austin-RitchieAffiliated withCambridge Bioscience
  • , B. BannerAffiliated withDepartment of Pathology, University Massachusetts Medical School
  • , C. HollinsIIIAffiliated withBASF
  • , C. MaramagAffiliated withDivision of Urologic and Transplantation Surgery, Department of Surgery, University of Massachusetts Medical School
  • , H. PriceAffiliated withDivision of Urology, University of Texas-Houston Medical School
  • , M. MenonAffiliated withDivision of Urologic and Transplantation Surgery, Department of Surgery, University of Massachusetts Medical School

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Abstract

To develop an autoimmune animal model for interstitial cystitis (IC), we injected rats with Freund's adjuvant (CFA) containing bladder homogenate (experimentals) or CFA alone (shams). We observed a doubling of urinary frequency in the experimental animals over the shams (P=0.004) and histopathologic changes (venular congestion) consistent with IC. Statistically significant bladder capacity changes were not found. Mast cell (MC) number was not statistically different between experimentals and controls but the number of MCs from section to adjacent section within the same animal's bladder did vary markedly, indicating that MC counts are not a reliable measure of disease in the rat bladder. Splenocytes cultured from the experimental animals and transferred to naive syngeneic recipients were capable of transferring the urinary frequency changes and vascular congestion while splenocytes from animals which did not develop the condition were without effect. In summary, we have developed an autoimmune model for IC consistent with the clinical features of IC. The features of this model can be transferred to naive syngeneic recipients via adoptive splenocyte transfer. The model will permit us to ask and answer important questions about the pathogenesis and treatment of the human disease.

Key words

Interstitial cystitis Animal model Urinary frequency Venular congestion