Department of Urology, Buddhist Tzu Chi General Hospital and Tzu Chi University, Hualien, Taiwan.
BJU Int. 2011 Jul;108(2 Pt 2):E136-41. doi: 10.1111/j.1464-410X.2010.09911.x. Epub 2010 Dec 16.
To investigate the relationships between suburothelial inflammation and urothelial dysfunction in interstitial cystitis/painful bladder syndrome (IC/PBlS).
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)).
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).
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.
探讨间质性膀胱炎/膀胱疼痛综合征（IC/PBS）中逼尿下层炎症与尿路上皮功能障碍的关系。
对 20 例 IC/PBS 患者和 6 例对照患者的膀胱组织进行 Ki-67（评估细胞增殖）、连接蛋白 E-钙黏蛋白、类胰蛋白酶（评估肥大细胞活化）和 TUNEL（评估尿路上皮细胞凋亡）免疫荧光染色。采用 ImageJ 方法测量 E-钙黏蛋白的荧光强度。测量并量化凋亡细胞、增殖细胞和活化肥大细胞的百分比，以每单位面积（4 µm²）的阳性细胞（±SD）表示。
与对照组相比，IC/PBS 患者膀胱组织中 Ki-67 阳性细胞的比例显著下调（0.559 ± 0.658 比 1.23 ± 1.28，P = 0.001）。TUNEL 染色显示，IC/PBS 膀胱组织中的凋亡细胞数量明显高于对照组（2.26 ± 2.04 比 0.051 ± 0.124，P = 0.000）。与对照组相比，IC/PBS 膀胱组织中的类胰蛋白酶信号明显更强（6.16 ± 4.35 比 1.15 ± 0.436，P = 0.000）。IC/PBS 膀胱组织中的凋亡细胞数量与肥大细胞活化显著相关（P = 0.021）。免疫荧光还显示，与对照组相比，IC/PBS 膀胱组织中 E-钙黏蛋白的分布明显减少（8.50 ± 6.83 比 17.2 ± 11.9，P = 0.000）。IC/PBS 膀胱组织中 E-钙黏蛋白表达降低与患者的视觉模拟疼痛评分显著相关（P = 0.008）。
本研究结果表明，IC/PBS 膀胱中的尿路上皮稳态受损，异常的尿路上皮功能与慢性炎症显著相关。IC/PBS 膀胱中的尿路上皮细胞之间的连接异常，与患者的自我报告疼痛量表相关。
