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Toll-like receptor 10 (TLR10) exhibits suppressive effects on inflammation of prostate epithelial cells

查看全文 作  者:Yu [1]Fan;Lu [1]Yang;Qiang [1]Wei;Yu [2]Ding;Zhuang [3]Tang;Ping [1]Tan;Tao [1]Lin;Duan [4]Guo;Shi [1]Qiu 高影响力作者 机构地区:[1]Department of Urology, Institute of Urology, West China Hospital of Sichuan University, Chengdu 610041, China;[2]Department of Core Facility, West China Hospital of Sichuan University, Chengdu 610041, China;[3]Department of Urology, Sun Yat-Sen Memorial Hospital of Zhongshan University, Guangzhou 510120, China;[4]Department of Palliative Medicine, West China Fourth Affiliated Hospital of Sichuan University, Chengdu 610041, China高影响力机构 出  处:《Asian Journal of Andrology》索引2019年第21卷第4期,共7页高影响力期刊 基  金:the National Key Research and Development Program of China (Grant No. SQ2017YFSF090096);National Natural Science Foundation of China (Grant No. 81370855,81770756 and 81300627);Foundation of Science and Technology Department of Sichuan Province (Grant No. 2013SZ0006, 2015SZ0230, 2018JY0089 and 2017HH0063);1.3.5 Project for Disciplines of Excellence, West China Hospital, Sichuan University (Grant No. ZY2016104);Youth Researcher Funding of Sichuan University (Grant No. 2017SCU11042 and 2017SCU04A17);Research Funding of Sichuan Health and Family Planning Commission (Grant No. 17PJ159,18PJ434 and 18PJ453). 摘  要:Prostate inflammation (PI) is closely related to the development and progression of chronic prostatic diseases: benign prostatic hyperplasia and prostate cancer. Toll-like receptor (TLR) 2 has been reported to be associated with inflammatory diseases, such as infections, autoimmune diseases, and cancers. Meanwhile, TLR10, which can form heterodimers with TLR2, has been considered an orphan receptor without an exact function. The present study therefore aims to examine the effects of TLR2 and TLR10 on PI. Prostate samples and clinical data were obtained from the patients diagnosed with benign prostatic hyperplasia. The inflammatory cell model was established by adding lipopolysaccharide to RWPE-1 cells. Prostate tissues/cells were examined by histological, molecular, and biochemical approaches. Both TLR2 and TLR10 were found to be expressed in prostate tissues and RWPE-1 cells. mRNA/protein expression levels of TLR2 and TLR10 were both positively correlated with prostate tissue inflammatory grades. Lipopolysaccharide-stimulated RWPE-1 cells expressed higher levels of TLR2, TLR10, high mobility group box 1 (HMGB1), phosphonuclear factor kappa-light-chain-enhancer of activated B-cells P65 (phospho-NF-κB P65), interleukin (IL)-6, and IL-8 than control cells. Moreover, HMGB1, phospho-NF-κB P65, IL-6, and IL-8 were down regulated after TLR2 knockdown and upregulated after TLR10 knockdown in RWPE-1 cells. TLR2 stimulation can activate the inflammatory signaling cascade in prostate epithelial cells. Conversely, TLR10 exhibited suppressive effects on inflammation. With antagonistic functions, both TLR2 and TLR10 were invoIved in PI. TLR10 could be a novel target in modulating inflammatory signal transduction of prostate epithelial cells. 关 键 词:benign PROSTATIC HYPERPLASIA INFLAMMATION TOLL-LIKE receptor 2 (TLR2) TLR10
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