Giri D, Ittmann M
Department of Pathology, Baylor College of Medicine, Houston, Texas, USA.
Am J Pathol. 2001 Jul;159(1):139-47. doi: 10.1016/S0002-9440(10)61681-1.
Benign prostatic hyperplasia (BPH) is an extremely common disease of older men in which there is benign overgrowth of the prostatic transition zone, leading to obstruction of urine outflow. Fibroblast growth factor (FGF) 2, a potent growth factor for prostatic stromal and epithelial cells, is increased twofold in BPH and its concentration is correlated with stromal proliferation in this condition. Immunohistochemistry of normal and hyperplastic prostate revealed that FGF2-expressing stromal cells were present in higher numbers near the epithelial acini, implying that epithelial cells may express a factor that induces FGF2 expression by stromal cells. Conditioned medium from primary cultures of prostatic epithelial cells was capable of inducing increased expression of FGF2 by primary stromal cultures. Blocking experiments with neutralizing anti-interleukin (IL)-8 antibodies and pretreatment with lipopolysaccharide, which down-regulates the IL-8 receptor, show that this inducing activity is because of the presence of IL-8 in the epithelial-conditioned medium. Analysis of normal prostatic peripheral zone and BPH tissue by enzyme-linked immunosorbent assay reveals that IL-8 is present at increased levels in hyperplastic prostate. Therefore IL-8 produced by prostatic epithelial cells can induce FGF2, a potent stromal and epithelial growth factor, and in this manner promote the abnormal proliferation of the prostatic transition zone that is critical in the pathogenesis of BPH.
良性前列腺增生(BPH)是老年男性极为常见的疾病,其前列腺移行区出现良性过度生长,导致尿液流出受阻。成纤维细胞生长因子(FGF)2是前列腺基质和上皮细胞的一种强效生长因子,在BPH中增加了两倍,且其浓度与这种情况下的基质增殖相关。对正常和增生前列腺进行免疫组织化学分析显示,表达FGF2的基质细胞在上皮腺泡附近数量更多,这意味着上皮细胞可能表达一种诱导基质细胞表达FGF2的因子。前列腺上皮细胞原代培养的条件培养基能够诱导原代基质培养物中FGF2表达增加。用中和抗白细胞介素(IL)-8抗体进行阻断实验以及用下调IL-8受体的脂多糖进行预处理表明,这种诱导活性是由于上皮条件培养基中存在IL-8。通过酶联免疫吸附测定对正常前列腺外周区和BPH组织进行分析发现,增生前列腺中IL-8水平升高。因此,前列腺上皮细胞产生的IL-8可诱导FGF2(一种强效的基质和上皮生长因子),并以此促进前列腺移行区的异常增殖,这在BPH发病机制中至关重要。