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Lymphocyte sub-populations in the bladder wall in normal bladder, bacterial cystitis and interstitial cystitis
1Department of Urology, Charing Cross Hospital, London, UK.
Insights
Interstitial cystitis (IC) bladder walls show increased CD4+, CD8+, and gamma delta T cells, along with IgA+, IgG+, and IgM+ plasma cells. These immune cells may contribute to the pathogenesis of IC.
Area of Science:
- Immunology
- Urology
- Pathology
Background:
- Interstitial cystitis (IC) is a chronic bladder condition with unknown etiology.
- Understanding the immune cell infiltrate in the bladder wall is crucial for elucidating IC pathogenesis.
Purpose of the Study:
- To identify and quantify lymphocyte sub-populations within the bladder wall of patients with IC, bacterial cystitis (BC), and normal controls.
Main Methods:
- Bladder biopsies were analyzed using immunofluorescent staining with monoclonal antibodies for T cell markers (CD3, CD4, CD8, TCRs) and plasma cell markers (IgA, IgG, IgM).
- Cellular location and numbers were determined, alongside peripheral blood lymphocyte counts.
Main Results:
- Patients with IC showed significantly higher numbers of CD4+, CD8+, and gamma delta T cells in the urothelium and submucosa compared to normal controls.
- T cell numbers in IC and BC patients were comparable, but gamma delta T cells were specifically associated with IC.
- Increased IgA+, IgM+, and IgG+ plasma cells were found in the urothelium and submucosa of IC patients, significantly more than in BC or control groups.
- Peripheral blood lymphocyte counts remained unchanged across all groups.
Conclusions:
- The elevated presence of CD4+, CD8+, gamma delta T cells, and plasma cells in the bladder wall of IC patients suggests their active role in the disorder's pathogenesis.
- Urothelial expression of HLA-DR and Class I molecules in IC may facilitate immune cell-mediated urothelial damage, leading to the end-stage pathology of IC.
Objective:
To identify lymphocyte sub-populations within the bladder wall in normal controls, in patients with bacterial cystitis (BC) or interstitial cystitis (IC).
Patients And Methods:
Bladder biopsies were taken from 21 patients with IC, four with BC and five normal controls. Immunofluorescent staining of biopsies was performed using monoclonal antibodies to the T cell markers CD3, CD4, CD8, TCR delta 1, delta TCS1, beta F1 and IML. Plasma cells were identified using monoclonal antibodies to IgA, IgG and IgM. The location and numbers of cells were determined. Peripheral blood lymphocyte counts were also performed in each case.
Results:
T cells (CD4+ and CD8+) were significantly more abundant within the bladder biopsies from patients with interstitial cystitis than in those from the normal controls, and were present within the urothelium and submucosa but not the detrusor. There was no difference between the numbers of T cells present in the biopsies from patients with interstitial cystitis and in those with bacterial cystitis. However, the presence of gamma delta T cells was significantly associated with interstitial cystitis. IgA+ and IgM+ plasma cells were located within the urothelium and submucosa but not the detrusor in patients with IC and the numbers present in these patients were significantly greater than in those with BC or the normal controls. The peripheral blood lymphocyte counts were not altered in any of the study cases.
Conclusion:
The increased numbers of CD4+, CD8+ and gamma delta cells as well as IgA+, IgG+ and IgM+ plasma cells within the urothelium and submucosa in patients with IC suggest that these cells play an active role in the pathogenesis of the disorder. The previously described abnormal urothelial expression of HLA-DR and hyperexpression of Class I molecules in patients with IC may enable these cells to cause destruction of the urothelium--the end stage of IC.