Activation of Nod1 and Nod2 induces innate immune responses of prostate epithelial cells - Abstract

BACKGROUND: Nod1 and Nod2 are cytosolic receptors which are responsible for sensing bacterial peptidoglycan derivatives.

In this study, we determined whether Nod1 and Nod2 are involved in the innate immune responses of prostate epithelial cells.

METHODS: The expression of Nod1 and Nod2 was examined by RT-PCR and immunohistochemistry. ELISA was performed to determine the production of cytokines/chemokines. Activation of NF-κB and MAPK was examined using western blot analysis.

RESULTS: The Nod1 gene was distinctly expressed in all tested cells including DU145, PC3, and TRAMP-C2 cells, whereas Nod2 expression was weak. Both Nod1 and Nod2 proteins were expressed in normal mouse prostate epithelia with difference of expression levels. Tri-DAP (Nod1 agonist), but not MDP (Nod2), increased the production of IL-8 (or KC) and IL-6 in prostate epithelial cells. Tri-DAP and MDP could upregulate the gene expression of COX-2 and activate NF-κB and MAPK. In addition, Tri-DAP and MDP synergized with TLR agonists to induce the production of IL-8/KC or IL-6 in PC3 and TRAMP-C2 cells. We finally showed that Nod1 and Nod2 were also expressed in a wide range of prostate lesions including prostate intraepithelial neoplasm (PIN), phyllodes-like tumor, and adenocarcinoma in TRAMP (transgenic adenocarcinoma of the mouse prostate) mice, even though the expression level of Nod1 and Nod2 was different.

CONCLUSION: These results indicate that Nod1 and Nod2 may play important roles in the innate immune response of prostate epithelial cells and the development and progression of prostate cancer.

Written by:
Kang MJ, Heo SK, Song EJ, Kim DJ, Han SY, Han JH, Kim BY, Park JH.   Are you the author?
Department of Biochemistry, College of Medicine, Konyang University, Daejeon, Korea; World Class Institute, Korea Research Institute of Bioscience and Biotechnology, Ochang-Eup, Cheongwon-Gun, Choongbuk, Korea.

Reference: Prostate. 2012 Jan 6.
doi: 10.1002/pros.22483. [Epub ahead of print]

PubMed Abstract
PMID: 22228081

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