Uchida K, Samma S, Rinsho K, Warren J R, Oyasu R
Department of Pathology, Northwestern University Medical School, Chicago, Illinois 60611.
J Urol. 1989 Oct;142(4):1122-6. doi: 10.1016/s0022-5347(17)39010-9.
Using heterotopically transplanted rat urinary bladder, experiments were conducted to develop a reproducible animal model of bacterial cystitis-associated urothelial hyperplasia without calculus formation, and to elucidate which bacterial component(s) might induce urothelial hyperplasia. Bladder instillation of live Escherichia coli (E. coli) resulted in persistent infection and inflammation and also diffuse urothelial hyperplasia. Instillation of killed E. coli also induced diffuse hyperplasia. Hyperplastic changes regressed following withdrawal of the killed E. coli treatment. Urothelial hyperplasia was also induced by repeated instillation of protein-rich lipopolysaccharide (LPS), the endotoxin derived from gram-negative bacterial wall component, but not by protein-free LPS. A finding common to bladders showing hyperplasia was the infiltration of neutrophils into intercellular spaces of the urothelium. We conclude that urothelial hyperplasia is induced by E. coli cystitis, that LPS plays a significant role in the hyperplastic response, and that neutrophils may mediate the response.
利用异位移植的大鼠膀胱，开展了实验以建立一种可重复的、不形成结石的细菌性膀胱炎相关膀胱上皮增生动物模型，并阐明哪些细菌成分可能诱导膀胱上皮增生。向膀胱内灌注活的大肠杆菌（E. coli）导致持续感染和炎症，以及弥漫性膀胱上皮增生。灌注灭活的大肠杆菌也诱导了弥漫性增生。在停止灭活大肠杆菌治疗后，增生性改变消退。富含蛋白质的脂多糖（LPS）（革兰氏阴性菌细胞壁成分衍生的内毒素）反复灌注也诱导了膀胱上皮增生，但无蛋白质的LPS则未诱导增生。显示增生的膀胱的一个共同发现是中性粒细胞浸润到膀胱上皮的细胞间隙中。我们得出结论，大肠杆菌膀胱炎诱导膀胱上皮增生，LPS在增生反应中起重要作用，并且中性粒细胞可能介导该反应。
