New therapy with ASC-J9 ® to suppress the prostatitis via altering the cytokine CCL2 signals

// Shin-Jen Lin 1 , Fu-Ju Chou 1 , Chang-Yi Lin 1 , Hong-Chiang Chang 1 , Shuyuan Yeh 1 , Chawnshang Chang 1, 2 1 George Whipple Laboratory for Cancer Research, Departments of Pathology, Urology, and Radiation Oncology, and Wilmot Cancer Center, University of Rochester Medical Center, Rochester, NY 14642, USA 2 Sex Hormone Research Center, China Medical University/Hospital, Taichung 404, Taiwan Correspondence to: Chawnshang Chang, email: chang@urmc.rochester.edu Keywords: prostate, ASC-J9 ® , CCL2 Received: March 23, 2016      Accepted: July 19, 2016      Published: August 22, 2016 ABSTRACT Prostatitis is a common disease contributing to 8% of all urologist visits. Yet the etiology and effective treatment remain to be further elucidated. Using a non-obese diabetes mouse model that can be induced by autoimmune response for the spontaneous development of prostatitis, we found that injection of the ASC-J9 ® at 75 mg/Kg body weight/48 hours led to significantly suppressed prostatitis that was accompanied with reduction of lymphocyte infiltration with reduced CD4 + T cells in prostate. In vitro studies with a co-culture system also confirmed that ASC-J9 ® treatment could suppress the CD4 + T cell migration to prostate stromal cells. Mechanisms dissection indicated that ASC-J9 ® can suppress CD4 + T cell migration via decreasing the cytokine CCL2 in vitro and in vivo , and restoring CCL2 could interrupt the ASC-J9 ® suppressed CD4 + T cell migration. Together, results from in vivo and in vitro studies suggest that ASC-J9 ® can suppress prostatitis by altering the autoimmune response induced by CD4 + T cell recruitment, and using ASC-J9 ® may help us to develop a potential new therapy to battle the prostatitis with little side effects.