Transmitters derived from vesical urothelium ? in association with the pathogenesis ofInterstitial Cystitis

本研究旨在阐明间质性膀胱炎（IC）的发病机制，这是一种病因不明的膀胱慢性炎症性疾病。为了达到这一目的，我们重点研究了尿路上皮上表达的递质或人类IC患者尿液中分泌的递质。同时，我们用免疫组织化学方法评估了膀胱组织学。不幸的是，到目前为止，尿液标志物与IC症状之间没有明显的相关性。然而，组织化学分析显示，在溃疡型IC中，表达CD11b和VEGF-A的免疫细胞明显增加。此外，在伴有干燥综合征的IC的膀胱组织中，CD4和CD8阳性免疫细胞均明显出现，这表明每种类型IC的发病机制不同。动物模型实验中，我们试图制作氯胺酮诱导的膀胱炎大鼠模型，但目前未产生IC症状的发现。用丙烯醛制备大鼠IC模型，测定膀胱组织中TRPM8的表达。大鼠尿频和排尿量发生动态变化，但TRPM8表达无明显变化。IC的发病机制和病理生理仍不明确，需要进一步研究。

This study was conducted to elucidate the pathogenesis of interstitial cystitis (IC), chronic inflammatory disease of the urinary bladder with unidentified cause. To achieve this purpose, we’ve focused on the transmitters expressed on urothelium or secreted into urine of human IC patients. Also, we’ve assessed bladder histology immuno-histochemically.Unfortunately, no significant correlation between urine markers and IC symptoms has been identified so far. However, histochemistry analysis indicated that immune cells expressing CD11b and VEGF-A significantly increased in ulcer type IC. In addition, in bladder tissue of IC with Sjogren’s syndrome showed significant appearance of both CD4 and CD8 positive immune cells, all of which indicating different pathogenesis in each type of IC.In animal model experiments, we tried to produce ketamine induced cystitis rat model, however, at the moment, IC symptoms of findings were not produced. Also we’ve produced rat IC model using acrolein,he bladder tissue of which was assessed for TRPM8 expression. The rats showed dynamic change in urinary frequency and voided volume, but no significant change in TRPM8 expression was observed.The pathogenesis and pathophysiology of IC are still undefined and need further investigations.