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Lymphocyte function in patients with interstitial cystitis
C H Miller1, J P MacDermott, K B Quattrocchi
1Department of Urology, University of California, Davis, Sacramento.
Insights
This study found no evidence of primary immune system dysfunction in interstitial cystitis patients. Urine did not stimulate immune cells, challenging autoimmune theories for this bladder condition.
Area of Science:
- Immunology
- Urology
Background:
- Interstitial cystitis (IC) etiology remains unclear.
- Autoimmune factors are hypothesized but lack direct evidence.
Purpose of the Study:
- To investigate potential primary immunological disorders in IC.
- To assess the immunogenic potential of urine in IC patients.
Main Methods:
- Compared in vitro peripheral blood lymphocyte function (proliferation, activation) between IC patients and healthy controls.
- Analyzed lymphocyte phenotypes (CD2, CD4, CD8, CD19, CD14, CD56), HLA-DR, and IL-2 receptor expression.
- Assessed cytokine production (IL-1, IL-2, IFN-γ) and urine's effect on lymphocyte activation.
Main Results:
- No significant differences in lymphocyte proliferation or activation between IC patients and controls.
- Autologous urine did not increase lymphocyte activation in either group.
- No differences in cytokine production (IL-1, IL-2, IFN-γ) were observed.
Conclusions:
- Results do not support a primary immunological disorder in IC.
- Urine does not appear to act as an immune stimulant in IC.
- Findings question autoimmune theories and the role of urinary autoantigens in IC pathogenesis.
Abstract:
To determine whether there is a primary immunological disorder involved in the etiology of interstitial cystitis, we compared the in vitro function of peripheral blood lymphocytes from 10 patients with interstitial cystitis to those from 10 healthy female controls. The lymphocytes were isolated and incubated in either cell culture medium alone, cell culture medium supplemented with the mitogen phytohemagglutinin or cell culture medium with autologous sterile filtered urine, the latter to detect any immunogenic potential of urine in this disease. We studied the relative proliferation of the phenotypes CD2, CD4, CD8, CD19, CD14 and CD56 by immunofluorescence and flow cytometry. To detect activation of T lymphocytes we also studied expression of HLA-Dr and interleukin-2 receptors. There was no difference in the rate of proliferation of the various lymphocyte phenotypes between the 2 groups in any of the culture media. Similarly, there was no difference between the 2 groups in the degree of lymphocytic activation after incubation. Furthermore, incubation in the presence of autologous urine caused no increase in activation above that seen in control cultures. We also assessed the production of the lymphokines interleukin-1, interleukin-2 and interferon-gamma in the supernatant fluid of the cell cultures. There was no difference in the production of these immunoregulatory cytokines between the control and patient groups, and again urine did not act as a mitogen in either group. We conclude from this study that there is no primary immunological disorder evident in patients with interstitial cystitis, and that the urine does not act as a stimulant to the immune system. This finding casts severe doubt on any theory suggesting that interstitial cystitis is an autoimmune disease or that urine contains an autoantigen causing the disease.