Center of Electron Microscopy, School of Medical Sciences, National University of Cordoba, Córdoba, Argentina.
Prostate. 2010 Aug;70(11):1153-65. doi: 10.1002/pros.21150.
It has been proposed that prostatic inflammation plays a pivotal role in the pathophysiology of benign hyperplasia and prostate cancer. However, little information is available about the prostatic reaction to bacterial compounds in vivo. Our aim was therefore to evaluate the early effects of bacterial infection on rat ventral prostate compartments.
Using a rat model of acute bacterial prostatitis by Escherichia coli, we analyzed the histological and ultrastructural changes in the prostate at 24, 48, and 72 hr postinfection. Prostatic tissues were immunostained for prostatic binding protein (PBP), ACTA2, ErbB1, and ErbB2 receptors, TUNEL, and markers of cell proliferation. Dot and Western blots for PBP, ACTA2, ErbB1, ErbB2, and TGFbeta1 were also performed.
The prostatic epithelium became hypertrophied, with increases in PBP and ErbB1 expression at 24 hr postinfection. Moreover, inflammation induced the expression of ErbB2, a receptor strongly involved in carcinogenesis. These alterations were more pronounced at 48 hr, but the epithelium also showed apoptosis and finally atrophy at 72 hr postinfection, with a decrease in PBP and ErbB receptors. Interestingly, the epithelial cells exhibited a high level of proliferation in response to the bacteria. The stromal reaction to acute inflammation was initially characterized by smooth muscle hypertrophy. Afterwards, muscle cells acquired a secretory phenotype, with a reduction in ACTA2 at 72 hr postinfection.
Prostatic inflammation, even at the early stages, promotes atrophic and proliferative changes, and the upregulation of ErbB receptors together with dedifferentiation of smooth muscle cells. These data suggest that repetitive reinfections could lead to uncontrolled growth in the prostate gland.
前列腺炎症被认为在良性前列腺增生和前列腺癌的病理生理学中起关键作用。然而，关于体内细菌化合物对前列腺的反应的信息很少。因此，我们的目的是评估细菌感染对大鼠前列腺腹侧叶的早期影响。
使用大肠杆菌诱导的大鼠急性细菌性前列腺炎模型，我们分析了感染后 24、48 和 72 小时前列腺的组织学和超微结构变化。前列腺组织用前列腺结合蛋白（PBP）、ACTA2、ErbB1 和 ErbB2 受体、TUNEL 和细胞增殖标志物进行免疫染色。还进行了 PBP、ACTA2、ErbB1、ErbB2 和 TGFbeta1 的点印迹和 Western blot。
前列腺上皮细胞增生，感染后 24 小时 PBP 和 ErbB1 表达增加。此外，炎症诱导了 ErbB2 的表达，ErbB2 是一种强烈参与致癌作用的受体。这些改变在 48 小时更为明显，但上皮细胞也在感染后 72 小时发生凋亡和最终萎缩，PBP 和 ErbB 受体减少。有趣的是，上皮细胞对细菌表现出高水平的增殖反应。急性炎症的间质反应最初表现为平滑肌肥大。随后，肌肉细胞获得分泌表型，感染后 72 小时 ACTA2 减少。
即使在早期，前列腺炎症也会促进萎缩和增殖变化，以及 ErbB 受体的上调和平滑肌细胞的去分化。这些数据表明，反复感染可能导致前列腺的失控生长。
