Interstitial cystitis is a chronic bladder disorder of unknown etiology that primarily afflicts women and is characterized by urgency and pain. Although immune mechanism have been implicated in the disease process, little is known about the local or peripheral blood immune responses. Cryostat sections of snap-frozen bladder biopsies obtained by transurethral resection from 43 patients (24 with classical and 9 with nonulcerative or early interstitial cystitis, and 10 controls) were analyzed using a panel of monoclonal antibodies with an avidin-biotin immunoperoxidase technique to characterize the local immune response of bladder mucosa. Simultaneously obtained heparinized peripheral blood (10 cc) was analyzed by flow cytometry in 24 patients (9 with classical and 5 with nonulcerative early interstitial cystitis, and 10 controls) using the same panel of antibodies. The control group biopsies (median age 44 years, range 27 to 52 years) had no ulcers, few lymphoid cells (predominately T-helper cells), rare T cell nodules and no B cells. The nonulcer group (median age 39 years, range 29 to 44 years) had rare mucosal ruptures but no ulcers, slightly increased lymphoid cells (predominately T-helper), occasional T cell aggregates, no B cell nodules and rare plasma cells. No statistically significant difference between control and nonulcerative interstitial cystitis patients was identified. In contrast, the classical interstitial cystitis group (median age 68 years, range 47 to 73 years) had ulcers, intense inflammation with focal sheets of plasma cells, aggregates of T cells, B cell nodules including germinal centers, a decreased or normal helper-to-suppressor cell ratio and suppressor cytotoxic cells in germinal centers. Flow cytometry analysis of peripheral blood lymphocyte subsets showed normal patterns in controls, increased numbers of secretory Ig positive B cells and activated lymphocytes in the nonulcerative group, and increased numbers of secretory Ig positive B cells with mildly abnormal kappa-to-lambda ratios and activated lymphocytes in the classical group. We conclude that an immune mechanism has at least a partial role in the pathophysiology of interstitial cystitis. A parallel between interstitial cystitis and inflammatory bowel disease is evident. Further studies are indicated.
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