Differential expression of interleukin-15, a pro-inflammatory cytokine and T-cell growth factor, and its receptor in human prostate

被引:59
|
作者
Handisurya, A [1 ]
Steiner, GE [1 ]
Stix, U [1 ]
Ecker, RC [1 ]
Pfaffeneder-Mantai, S [1 ]
Langer, D [1 ]
Kramer, G [1 ]
Memaran-Dadgar, N [1 ]
Marberger, M [1 ]
机构
[1] Univ Vienna, Urol Res Lab, Dept Urol, A-1090 Vienna, Austria
来源
PROSTATE | 2001年 / 49卷 / 04期
关键词
interleukin-15; receptor; benign prostatic hyperplasia; prostate cancer;
D O I
10.1002/pros.10020
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
BACKGROUND. Pro-inflammatory interleukin (IL)-15 plays a major role in host defense and chronic inflammation by stimulating T-lymphocyte recruitment and growth. Expression of IL-15 and IL-15 receptor (IL-15R) in human prostate was examined. METHODS. Normal and benign hyperplastic (BPH) prostate specimens (n = 23) were analyzed for IL-15 and IL-15R alpha -chain expression by immunohistochemistry and Real-Time-PCR/RT-PCR. Regulation of prostatic stromal cell (PSC) IL-15 mRNA and effect of IL-15 on prostatic cell growth were analysed in vitro. RESULTS. In normal prostate, anti-IL-15 and anti-IL-15R alpha -chain reactivity were restricted to smooth muscle and stromal cells. However, in BPH, in addition epithelial cells frequently exhibited discrete anti-IL-15R and often intense, membranous anti-IL-15 reactivity. IL-15/IL-15R mRNA were detected in all prostatic cells types. In BPH tissues, IL-15 mRNA content was variable (15-fold). IL-15 mRNA synthesis of PSC was significantly up-regulated by IFN-gamma. Furthermore IL-15 strongly stimulated the growth of BPH-T-lymphocytes and weakly that of carcinoma cell lines, but not of stromal cells. CONCLUSIONS. Overexpression of IL-15 and IL-15Ra-chain in BPH and massive proliferation of BPH-T-lymphocytes induced by IL-15 suggest a role for IL-15 in prostatic inflammation. Since IFN-gamma, a T-lymphocyte product, stimulates prostatic IL-15 production; chronic inflammation might be triggered by this paracrine loop. (C) 2001 Wiley-Liss, Inc.
引用
收藏
页码:251 / 262
页数:12
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