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What’s known on the subject? and What does the study add? Interstitial cystitis/painful bladder syndrome (IC/PBS) is considered to result from long‐standing inflammation of the bladder. Urothelial dysfunction and increased urothelial permeability are known to result in clinical symptoms such as pain and urgency, however the actual pathophysiology remains unclear. This study demonstrated increased cell apoptosis, decreased cell proliferation, increased mast cell activation, and impaired expression of E‐cadherin were significant in IC/PBS bladders. There was a significant correlation between mast cell activation and urothelial cell apoptosis and the reduced E‐cadherin expression was significantly correlated with clinical pain VAS scale, suggesting the barrier defect of the bladder wall may lead to increasing bladder sensitivity and pain. OBJECTIVE • To investigate the relationships between suburothelial inflammation and urothelial dysfunction in interstitial cystitis/painful bladder syndrome (IC/PBlS). MATERIALS AND METHODS • Immunofluorescence staining of ki‐67 (to assess cell proliferation), junction protein E‐cadherin, tryptase (to assess mast cell activation) and TUNEL (to assess urothelial apoptosis) were performed in bladder tissues from 20 patients with IC/PBlS and from 6 control patients. • The fluorescence intensity of E‐cadherin was measured using the ImageJ method. • The percentage of apoptotic cells, proliferated cells and activated mast cells were measured and quantified as positive cells (±SD) per area unit (4 µm 2 ). RESULTS • The ratio of ki‐67‐positive cells in the bladder tissue of the patients with IC/PBlS was significantly down‐regulated compared with that of the control patients (0.559 ± 0.658 vs. 1.23 ± 1.28, P = 0.001). • TUNEL staining revealed a significantly higher number of apoptotic cells in the IC/PBlS bladder tissue compared with control bladder tissue (2.26 ± 2.04 v 0.051 ± 0.124, P = 0.000). • The tryptase signal was significantly stronger in the IC/PBlS bladder tissue compared with that of control patients (6.16 ± 4.35 v 1.15 ± 0.436, P = 0.000). • The apoptotic cell number in IC/PBlS bladder tissue correlated significantly with mast cell activation ( P = 0.021). • Immunofluorescence also showed a significantly lower distribution of E‐cadherin in IC/PBlS bladder tissue compared with that of control patients (8.50 ± 6.83 v 17.2 ± 11.9, P = 0.000). • Lower expression of E‐cadherin in IC/PBlS bladder tissue was significantly correlated with higher visual analogue pain scores in patients with IC/PBlS ( P = 0.008). CONCLUSIONS • The results of the present study suggest that urothelial homeostasis in IC/PBlS bladders was impaired, and abnormal urothelial function was significantly associated with chronic inflammation. • The junctions between urothelial cells in IC/PBlS bladders were abnormal, which was associated with the patient’s self‐report pain scales.
Shie et al. (Thu,) studied this question.