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


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

Correspondence Address:
Qiang Wei,
Department of Urology, Institute of Urology, West China Hospital of Sichuan University, Chengdu 610041, China

Tao Lin,
Department of Urology, Institute of Urology, West China Hospital of Sichuan University, Chengdu 610041, China

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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/aja.aja_100_18

PMID: 30618413

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), phospho-nuclear 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 downregulated 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 involved in PI. TLR10 could be a novel target in modulating inflammatory signal transduction of prostate epithelial cells.


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